Acute peripheral facial palsy usually manifests Bell's palsy of unknown cause, and rarely lacunar infarct which located in facial nucleus can mimic peripheral facial palsy. A 73 year-old man with isolated facial asymmetry diagnosed with lacunar infarction which selectively involve the facial fascicles which lie in inferolateral aspect of pons. Clinicians should take into account the possibility of central lesion and brain stem infarction, even when patients present with isolated peripheral type facial palsy.
Bell Palsy ; Brain Stem Infarctions ; Facial Asymmetry ; Facial Nucleus ; Facial Paralysis* ; Humans ; Pons ; Stroke, Lacunar

BACKGROUND AND PURPOSE: During Vietnam War, many Korean soldiers were dispatched to fight in the war where they were exposed to Agent Orange. Until now, there exist only limited evidence on existence of association between exposure to Agent Orange and Parkinson's disease (PD). To elucidate the effects of Agent Orange exposure on PD, we compared the clinical characteristics and radiolabeled 18F-FP-CIT PET uptake between patients with Agent Orange exposure and patients with Agent Orange no-exposure. METHODS: We retrospectively evaluated 143 patients exposed to Agent Orange and 500 patients with no exposure to Agent Orange from our movement clinics database. The differences between clinical characteristics and pattern of 18F-FP-CIT PET uptake were investigated. RESULTS: Among Unified Parkinson's Disease Rating Scale III motor subscales, tremor at rest, rigidity, finger taps, and rapid alternating movement was significantly higher in patients exposed to Agent Orange as compared to patients with no exposure to Agent Orange. The facial expression score was significantly lower in patients exposed to Agent Orange as compared to patients with no exposure to Agent Orange. Compared to patients not exposed to Agent Orange, all basal ganglia areas (contra- and ipsilateral caudate nucleus, anterior putamen, and posterior putamen) showed a lower18F-FP-CIT uptake and higher asymmetry index of anterior and posterior putamen was found in patients exposed to Agent Orange. The caudate/putamen ratio was significantly lower in patients exposed to Agent Orange as compared to patients with no exposure to Agent Orange. CONCLUSIONS: This study showed a different clinical profile and FP-CIT PET findings between patients exposed to Agent Orange as compared to patients with no exposure to Agent Orange. This finding suggests the possibility of different pathophysiology of PD in patients exposed to Agent Orange from idiopathic PD.
Basal Ganglia ; Caudate Nucleus ; Citrus sinensis* ; Facial Expression ; Fingers ; Humans ; Military Personnel ; Parkinson Disease* ; Putamen ; Retrospective Studies ; Tremor ; Vietnam

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

The generally accepted taste pathway in an animal projects ipsilaterally from the solitary nucleus. However, the path-way of gustatory fibers in the human brainstem has not been sufficiently clarified. A 57-year-old hypertensive man was admitted with sudden dizziness and hemiageusia. A neurological examination revealed also a diminution of taste on the left half of his tongue. A MRI showed a high signal intensity in the right lower pontine area. This case suggests that the unilateral lesion of the pons may lead to contralateral taste disturbances.
Ageusia ; Animals ; Brain Stem ; Cerebral Infarction ; Dizziness ; Facial Nerve ; Humans ; Infarction* ; Magnetic Resonance Imaging ; Middle Aged ; Neurologic Examination ; Pons ; Solitary Nucleus ; Tongue

In the rat brain stem, the nerves innervating sublingual gland was studied with submandibular gland together. Cholera Toxin B subunit (CTB), neural tracer, is not yet used to study the sublingual gland. The purpose of this study is to investigate the origin of neurons and afferent fibers projecting to sublingual gland by means of retrograde transport of CTB. CTB was injected into the sublingual gland. In the rat brain stem, neurons were labeled with CTB in superior salivatory nucleus (SSN), inferior salivatory nucleus (ISN), facial nucleus and their afferent fibers in nucleus tractus solitarius. At the rostal level of SSN, the labeled cells were found in lateral aspect of pontine reticular formation. At the level of facial nerve that transverse the dorsal part of the spinal trigeminal tract, the labeled cells of SSN extended in the area of facial nerve fibers. Labeled cells were also seen at the level of internal genu of facial nerve. In ISN at the level of facial nerve that traverse the dorsal part of the spinal trigeminal tract, the labeled cells were seen in the anterolateral direction of lateral aspect of reticular formation. In the facial nucleus, the labeled cells were confined in central part of facial nucleus. The labeled nerve fibers in nucleus tractus solitarius were seen in the level at which the medial border of the nucleus tractus solitarius meets the 4th ventricle.
Animals ; Brain Stem* ; Brain* ; Cholera Toxin* ; Cholera* ; Facial Nerve ; Immunohistochemistry ; Nerve Fibers ; Neurons ; Rats* ; Reticular Formation ; Solitary Nucleus ; Sublingual Gland* ; Submandibular Gland

Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterized by a deficit in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures in the first 3 years of life. It is not a single disorder, and it is broadly considered to be a multi-factorial disorder resulting from genetic and non-genetic risk factors and their interaction. Genetic studies of ASD have identified mutations that interfere with typical neurodevelopment in utero through childhood. These complexes of genes have been involved in synaptogenesis and axon motility. Recent developments in neuroimaging studies have provided many important insights into the pathological changes that occur in the brain of patients with ASD in vivo. Especially, the role of amygdala, a major component of the limbic system and the affective loop of the cortico-striatothalamo-cortical circuit, in cognition and ASD has been proved in numerous neuropathological and neuroimaging studies. Besides the amygdala, the nucleus accumbens is also considered as the key structure which is related with the social reward response in ASD. Although educational and behavioral treatments have been the mainstay of the management of ASD, pharmacological and interventional treatments have also shown some benefit in subjects with ASD. Also, there have been reports about few patients who experienced improvement after deep brain stimulation, one of the interventional treatments. The key architecture of ASD development which could be a target for treatment is still an uncharted territory. Further work is needed to broaden the horizons on the understanding of ASD.
Amygdala ; Autistic Disorder* ; Axons ; Brain ; Child ; Autism Spectrum Disorder* ; Cognition ; Deep Brain Stimulation ; Facial Expression ; Gestures ; Humans ; Limbic System ; Neurobiology ; Neuroimaging ; Nucleus Accumbens ; Reward ; Risk Factors ; Social Behavior

The purpose of this study is to investigate the origin of neurons and afferent fibers projecting to submandibular gland by means of retrograde transport of Cholera Toxin B Subunit (CTB). CTB was injected into the both side submandibular gland or left side submandibular gland. In the rat brain stem, neurons were labeled with CTB in superior salivatory nucleus (SSN), facial nucleus, caudal region of hypoglossal nucleus, lateral horn of spinal cervical segment and their afferent fibers in nucleus tractus solitarius. At the most rostal level of SSN, the labeled cells were seen in lateral aspect of pontine reticular formation. At the level of facial nerve that traverse the dorsal part of the spinal trigeminal tract, the labeled cells of SSN extended to the anterolateral direction of lateral aspect of reticular formation. At the level of facial nucleus, the labeled cells of SSN were seen in the area of caudal prologation of the same region of rostral ones, but decreased in cell number. In the facial nucleus, the labeled cells were confined in central part of facial nucleus. In the first and second spinal cervical segment, the labeled cells were seen in the intermediomedial nucleus of lateral horn. The labeled nerve fibers in nucleus tractus solitarius were seen at the level of the 4th ventricle which the medial border of the nucleus tractus solitarius meets. Injection of CTB into the left submandibular gland labeled their neurons on the left and right superior salivatory nucleus (SSN), but other labeled cells and fibers were localized only on the left side.
Animals ; Brain Stem* ; Brain* ; Cell Count ; Cholera Toxin* ; Cholera* ; Facial Nerve ; Horns ; Immunohistochemistry ; Nerve Fibers ; Neurons ; Rats* ; Reticular Formation ; Solitary Nucleus ; Submandibular Gland*

BACKGROUND AND OBJECTIVES: The transsynaptic transfer of neurotropic viruses is an effective tool for tracing chains of connected neurons, because replication of virus in the recipient neurons after the transfer amplifies the "tracer signal". The aim of this study is to identify the central neural pathways projecting to the facial nerve using the Bartha strain of the Pseudorabies virus (PRV-Ba )as a transsynaptic tracer. MATERIALS AND METHODS: PRV-Ba was injected into the facial nerve in the stylomastoid foramen of a rat, and was localized in the rat brain with light microscopic immunohistochemistry using primary antibodies against the PRV-Ba. Sequential tracing was carried out on the retrogradely labeled neurons were done. RESULTS: The shapes of upper motor neurons of facial nerve were mostly ovoid or polygonal. The positive immunoreactive cells observed in the brainstem nuclei included raphe obscurus nucleus, facial nucleus, parvocellular reticular nucleus, spinal trigeminal nucleus, ventral parabrachial nucleus, central gray, and dorsal raphe nucleus. Other positive cells stained in the diencephalon were found in periventricular hypothalamic nucleus, dorsal hypothalamic area, orbital gyri, and infralimbic cortex in the frontal lobe. CONCLUSIONS: These results show the central neural pathways of facial nerve using PRV-Ba.
Animals ; Antibodies ; Brain ; Brain Stem ; Diencephalon ; Facial Nerve ; Frontal Lobe ; Herpesvirus 1, Suid ; Immunohistochemistry ; Motor Neurons ; Neural Pathways* ; Neurons ; Orbit ; Raphe Nuclei ; Rats ; Trigeminal Nucleus, Spinal

In the rat brain stem, the origin of neurons and afferent fibers projecting to the lacrimal, submandibular or sublingual gland was investigated by means of retrograde transport of Cholera Toxin B Subunit (CTB), respectively. Injection of CTB into the lacrimal gland labeled their neurons in superior salivatory nucleus (SSN) and facial nucleus. Superior salivatory neurons innervating lacrimal gland were labeled more densely in the rostral and caudal part of SSN. In the facial nucleus, labeled cell bodys were seen in the posterolateral part of facial nucleus. Injection of CTB into the submandibular or sublingual gland labeled their neurons in SSN and their afferent fibers in nucleus tractus solitarius (NTS). The superior salivatory neurons innervating submandibular or sublingual gland were labeled densely in the middle part of SSN. In the middle part of SSN, neurons innervating submandibular gland were labeled diffusely in the medial part of facial nerve and neurons innervating sublingual gland were labeled in the anteromedial and posterior part of facial nerve. The labeled nerve fibers in NTS were seen in the middle part of NTS.
Animals ; Brain Stem* ; Brain* ; Cholera Toxin* ; Cholera* ; Facial Nerve ; Lacrimal Apparatus ; Nerve Fibers ; Neurons ; Rats* ; Solitary Nucleus ; Sublingual Gland* ; Submandibular Gland

OBJECTIVEPPTA and c-fos mRNA expression were detected in dog caudalis subnucleus of trigeminal spinal tract nucleus (VC) induced by trauma occlusion in order to investigate orofacial pain mechanism.

METHODSThe occlusal surface of the first and second maxillary right molars in 15 dogs were unilaterally raised 1.5 mm with casting Ni-Cr inlay which were fixed in Class I hole. On days 3, 7, 14, 30 and 60 after teeth operation, the VC of right and left sides were removed. PPTA and c-fos mRNAs were detected in experimental and control groups with reverse transcription-polymerase chain reaction (RT-PCR).

RESULTS(1) The basal levels of PPTA and c-fos mRNAs were extremely low and poorly detectable in VC in control animals. (2) The expression of PPTA mRNA in VC of traumatic side was up regulated from 3 days after inlay was fixed in molar and reached peak level during 14 to 30 days and then down-regulated gradually and no significant difference was noted between 60 days group and control group. (3) c-fos mRNA expression was more intense during 3 to 7 days compared with the control group but undetectable in the other experimental period. (4) Both PPTA and c-fos mRNAs expression in VC of trauma occlusal side were more intense than that in the contralateral side.

CONCLUSIONSThe present results show that both PPTA and c-fos mRNA expression are elevated in dog's VC induced by traumatic occlusion. The primary afferent terminal of orofacial area is sensitized, which suggest one kind of mechanism of orofacial pain in the condition of traumatic occlusion.

Animals ; Dental Occlusion, Traumatic ; physiopathology ; Dogs ; Facial Neuralgia ; etiology ; Protein Precursors ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-fos ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; Tachykinins ; biosynthesis ; genetics ; Trigeminal Nucleus, Spinal ; metabolism