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Journal of Pharmacy & Bioallied Sciences 2017Marfan syndrome (MFS) is the autosomal dominant-inherited multisystem connective-tissue disorder, with a reported incidence of 1 in 10,000 individuals and equal...
Marfan syndrome (MFS) is the autosomal dominant-inherited multisystem connective-tissue disorder, with a reported incidence of 1 in 10,000 individuals and equal distribution in both genders. The main clinical manifestation of this disorder consists of an exaggerated length of the upper and lower limbs, hyperlaxity, scoliosis, alterations in the cardiovascular and pulmonary systems, and atypical bone overgrowth. Orofacial manifestations such as high-arched palate, hypodontia, long narrow teeth, bifid uvula, mandibular prognathism, and temporomandibular disorders are also common. Early diagnosis of MFS is essential to prevent the cardiovascular complications and treatment of orofacial manifestations, thus to increase the quality of life of the patient.
PubMed: 28584496
DOI: 10.4103/jpbs.JPBS_326_16 -
Indian Journal of Endocrinology and... 2020A complete examination of the oral cavity is a neglected part of physical examination and is not taught in both undergraduate and postgraduate medical training. We... (Review)
Review
A complete examination of the oral cavity is a neglected part of physical examination and is not taught in both undergraduate and postgraduate medical training. We believe that a thorough oral examination helps in the identification of a variety of endocrine disorders and so to emphasize this, we have proposed the term "orocrinolgy." Orocrinology is the art of using a Thorough oral cavity examination to diagnose a variety of adult and pediatric endocrine disorders. Under "orocrinology," we have highlighted an easy to perform a seven-step technique to perform a complete examination of the oral cavity. The common endocrine-related abnormalities that you might encounter during each of these seven steps is summarized along with the steps. The seven steps start with the examination of the salivary glands, followed by the lips. This is followed by the examination of labial, buccal, alveolar, and gingival mucosa in two steps. The fifth step is the Inspection of the tongue and the base of the mouth followed by the sixth step, which is the evaluation of the palate, uvula, and tonsils. The final seventh step is the examination of the hard structures in the oral cavity, which includes the teeth, mandible, and the maxilla.
PubMed: 33083263
DOI: 10.4103/ijem.IJEM_119_20 -
NeuroImage Dec 2022All volitional movement in a three-dimensional space requires multisensory integration, in particular of visual and vestibular signals. Where and how the human brain...
All volitional movement in a three-dimensional space requires multisensory integration, in particular of visual and vestibular signals. Where and how the human brain processes and integrates self-motion signals remains enigmatic. Here, we applied visual and vestibular self-motion stimulation using fast and precise whole-brain neuroimaging to delineate and characterize the entire cortical and subcortical egomotion network in a substantial cohort (n=131). Our results identify a core egomotion network consisting of areas in the cingulate sulcus (CSv, PcM/pCi), the cerebellum (uvula), and the temporo-parietal cortex including area VPS and an unnamed region in the supramarginal gyrus. Based on its cerebral connectivity pattern and anatomical localization, we propose that this region represents the human homologue of macaque area 7a. Whole-brain connectivity and gradient analyses imply an essential role of the connections between the cingulate sulcus and the cerebellar uvula in egomotion perception. This could be via feedback loops involved updating visuo-spatial and vestibular information. The unique functional connectivity patterns of PcM/pCi hint at central role in multisensory integration essential for the perception of self-referential spatial awareness. All cortical egomotion hubs showed modular functional connectivity with other visual, vestibular, somatosensory and higher order motor areas, underlining their mutual function in general sensorimotor integration.
Topics: Humans; Brain Mapping; Photic Stimulation; Magnetic Resonance Imaging; Cerebral Cortex; Brain
PubMed: 36334557
DOI: 10.1016/j.neuroimage.2022.119715 -
Journal of the ASEAN Federation of... 2023
Topics: Humans; Uvula; Cleft Palate; Hypopituitarism
PubMed: 37252424
DOI: 10.15605/jafes.038.01.18 -
Archives of Craniofacial Surgery Aug 2014A 14-month-old child was diagnosed with a Veau Class II cleft palate. Von Langenbeck palatoplasty was performed for the right palate, and V-Y pushback palatoplasty was...
A 14-month-old child was diagnosed with a Veau Class II cleft palate. Von Langenbeck palatoplasty was performed for the right palate, and V-Y pushback palatoplasty was performed for the left palate. The child did not have a special problem during the surgery, and the authors were able to elongate the cleft by 10 mm. Contrary to preoperative concerns regarding the hybrid use of palatoplasties, the uvula and midline incisions remained balanced in the middle. The authors named this combination method "half-and-half palatoplasty" and plan to conduct a long-term follow up study as a potential solution that minimizes the complications of palatoplasty.
PubMed: 28913201
DOI: 10.7181/acfs.2014.15.2.105 -
Taiwan Journal of Ophthalmology 2021Idiopathic intracranial hypertension (IIH) is a disorder of unknown etiology that results in isolated raised intracranial pressure. Classic symptoms and signs of IIH... (Review)
Review
Idiopathic intracranial hypertension (IIH) is a disorder of unknown etiology that results in isolated raised intracranial pressure. Classic symptoms and signs of IIH include headache, papilledema, diplopia from sixth nerve palsy and divergence insufficiency, and pulsatile tinnitus. Atypical presentations include: (1) highly asymmetric or even unilateral papilledema, and IIH without papilledema; (2) ocular motor disturbances from third nerve palsy, fourth nerve palsy, internuclear ophthalmoplegia, diffuse ophthalmoplegia, and skew deviation; (3) olfactory dysfunction; (4) trigeminal nerve dysfunction; (5) facial nerve dysfunction; (6) hearing loss and vestibular dysfunction; (7) lower cranial nerve dysfunction including deviated uvula, torticollis, and tongue weakness; (8) spontaneous skull base cerebrospinal fluid leak; and (9) seizures. Although atypical findings should raise a red flag and prompt further investigation for an alternative etiology, clinicians should be familiar with these unusual presentations.
PubMed: 33767953
DOI: 10.4103/tjo.tjo_69_20 -
Journal of Pharmacy & Bioallied Sciences Jul 2023Facial development involves an intricate regulatory mechanism that accounts for numerous craniofacial abnormalities, common being orofacial clefts. Although cleft in the...
Facial development involves an intricate regulatory mechanism that accounts for numerous craniofacial abnormalities, common being orofacial clefts. Although cleft in the secondary palate accounts for one-third of orofacial clefts stills remains an under-researched domain. Hence, in this work, the authors put forth two non-syndromic, asymptomatic cleft uvulae reported among bimodal male patients of the Indian-Asiatic population who came up for dental screening. Most of the time, isolated/asymptomatic cleft uvula patients will be reluctant to further investigations and treatment. Although bifid uvula looks benign in most patients, it may sometimes be associated with catastrophic complications. To conclude, whenever bifid uvula is an incidental finding, it is the responsibility of the healthcare worker to plan a thorough patient workup as a primary preventive measure to rule out any complications whenever feasible. It can help us overcome many future unforeseen sequelae and emergency management due to bifid uvula.
PubMed: 37654280
DOI: 10.4103/jpbs.jpbs_464_22 -
Frontiers in Neurology 2021Vestibular and optokinetic space is represented in three-dimensions in vermal lobules IX-X (uvula, nodulus) and hemisphere lobule X (flocculus) of the cerebellum. Vermal... (Review)
Review
Vestibular and optokinetic space is represented in three-dimensions in vermal lobules IX-X (uvula, nodulus) and hemisphere lobule X (flocculus) of the cerebellum. Vermal lobules IX-X encodes gravity and head movement using the utricular otolith and the two vertical semicircular canals. Hemispheric lobule X encodes self-motion using optokinetic feedback about the three axes of the semicircular canals. Vestibular and visual adaptation of this circuitry is needed to maintain balance during perturbations of self-induced motion. Vestibular and optokinetic (self-motion detection) stimulation is encoded by cerebellar climbing and mossy fibers. These two afferent pathways excite the discharge of Purkinje cells directly. Climbing fibers preferentially decrease the discharge of Purkinje cells by exciting stellate cell inhibitory interneurons. We describe instances adaptive balance at a behavioral level in which prolonged vestibular or optokinetic stimulation evokes reflexive eye movements that persist when the stimulation that initially evoked them stops. Adaptation to prolonged optokinetic stimulation also can be detected at cellular and subcellular levels. The transcription and expression of a neuropeptide, corticotropin releasing factor (CRF), is influenced by optokinetically-evoked olivary discharge and may contribute to optokinetic adaptation. The transcription and expression of microRNAs in floccular Purkinje cells evoked by long-term optokinetic stimulation may provide one of the subcellular mechanisms by which the membrane insertion of the GABAA receptors is regulated. The neurosteroids, estradiol (E2) and dihydrotestosterone (DHT), influence adaptation of vestibular nuclear neurons to electrically-induced potentiation and depression. In each section of this review, we discuss how adaptive changes in the vestibular and optokinetic subsystems of lobule X, inferior olivary nuclei and vestibular nuclei may contribute to the control of balance.
PubMed: 33767662
DOI: 10.3389/fneur.2021.635259 -
Internal Medicine (Tokyo, Japan) Dec 2017
PubMed: 29021463
DOI: 10.2169/internalmedicine.8898-17