Peripheral Cranial Nerve Research Articles

A narrative review on cervical artery dissection-related cranial nerve palsies.

This study aimed to emphasize the importance of cranial nerve (CN) palsies in spontaneous cervical artery dissection (sCeAD). A search term-based literature review was conducted on "cervical artery dissection" and "cranial nerve palsy." English and German articles published until October 2023 were considered. Cranial nerve (CN) palsy in sCeAD is evident in approximately 10% of cases. In the literature, isolated palsies of CN II, III, VII, IX, X, and XII have been reported, while CN XI palsy only occurs in combination with other lower cranial nerve palsies. Dissection type and mural hematoma localization are specific to affected CN as CN palsies of II or III are solely evident in those with steno-occlusive vessel pathologies located at more proximal segments of ICA, while those with CN palsies of IX, X, XI, and XII occur in expansive sCeAD at more distal segments. This dichotomization emphasizes the hypothesis of a different pathomechanism in CN palsy associated with sCeAD, one being hypoperfusion or microembolism (CN II, III, and VII) and the other being a local mass effect on surrounding tissue (CN IX, X, XI, and XII). Clinically, the distinction between peripheral palsies and those caused by brainstem infarction is difficult. This differentiation is key, as, according to the reviewed cases, peripheral cranial nerve palsies in sCeAD patients mostly resolve completely over time, while those due to brainstem stroke do not, making cerebrovascular imaging appraisal essential. It is important to consider dissections as a potential cause of peripheral CN palsies and to be aware of the appropriate diagnostic pathways. This awareness can help clinicians make an early diagnosis, offering the opportunity for primary stroke prevention.

Osteoclast activity sculpts craniofacial form to permit sensorineural patterning in the zebrafish skull.

Efforts to understand the morphogenesis of complex craniofacial structures have largely focused on the role of chondrocytes and osteoblasts. Along with these bone-creating cells, bone-resorbing osteoclasts are critical in homeostasis of adult skeletal structures, but there is currently limited information on their role in the complex morphogenetic events of craniofacial development. Fundamental aspects of skull formation and general skeletal development are conserved from zebrafish to mammals. Using a cathepsinK reporter, we documented osteoclast location in the developing zebrafish skull over several weeks, from 5.18mm to 9.6mm standard length (approximately 15 to 34 days post fertilization). While broad distribution of osteoclasts is consistent across individuals, they are sparse and the exact locations vary among fish and across developmental time points. Interestingly, we observed osteoclasts concentrating at areas associated with neuromasts and their associated nerves, in particular the hyomandibular foramina and around the supraorbital lateral line. These are areas of active remodeling. In contrast, other areas of rapid bone growth, such as the osteogenic fronts of the frontal and parietal bones, show no particular concentration of osteoclasts, suggesting that they play a special role in shaping bone near neuromasts and nerves. In csf1ra mutants lacking functional osteoclasts, the morphology of the cranial bone was disrupted in both areas. The hyomandibular foramen is present in the initial cartilage template, but after the initiation of ossification, the diameter of the canal is significantly smaller in the absence of osteoclasts. The diameter of the supraorbital lateral line canals was also reduced in the mutants, as was the number of pores associated with neuromasts, which allow for the passage of associated nerves through the bone. Our findings define important and previously unappreciated roles for osteoclast activity in shaping craniofacial skeletal structures with a particular role in bone modeling around peripheral cranial nerves, providing a scaffold for wiring the sensioneural system during craniofacial development. This has important implications for the formation of the evolutionarily diverse lateral line system, as well understanding the mechanism of neurologic sequelae of congenital osteoclast dysfunction in human craniofacial development.

Neonate with Respiratory Distress, Bilateral Microtia, Hypocalcemia, and Lymphopenia.

Neonate with Respiratory Distress, Bilateral Microtia, Hypocalcemia, and Lymphopenia.

Focal Peripheral Neuropathy Associated with Lymphoma in Dogs

Background: Peripheral neuropathies result in sensory, motor or autonomic dysfunctions due to impairment of peripheral spinal or cranial nerves. Neoplasms such as lymphoma are cited as one of the many aetiological causes and it may affect the nerve directly, by compression, or indirectly, or paraneoplastic, by remote action of the neoplasm located in an extra-neural site. This study aimed to report two cases of cranial nerve neuropathy (trigeminal and facial) associated with canine lymphoma, contributing to a better understanding of its paraneoplastic effects on the nervous system, as well as the diagnosis and treatment of these conditions.Cases: Two cases of canine lymphoma associated with possible signs of paraneoplastic peripheral neuropathy were attended at the Veterinary Hospital from the Universidade Federal de Minas Gerais (HV UFMG). Case 1. A spayed mixed breed bitch, with lethargy and unilateral exophthalmos. Brain computed tomography revealed a retrobulbar mass and cytology was diagnostic for extranodal lymphoma. Subsequent to computed tomography, the dog was presented with hypotrophy of the facial musculature and difficulty in grasping food, consistent with trigeminal nerve palsy, which resolved after institution of the 19-week chemotherapy protocol from the University of Wisconsin. Nevertheless, disease reccurred and a rescue protocol was initiated. Case 2. A female Dalmatian, spayed, was diagnosed with multicentric lymphoma, after cytology of the left mandibular lymph node. Chemotherapy was initiated with the same protocol of the previous case. However, the disease progressed and it was observed facial asymmetry with ptosis of the left eyelid, pina and lips, in addition to difficulty in grasping food, suggesting facial and trigeminal cranial nerve palsy. Clinical signs resolved after institution of a rescue chemotherapy protocol. However, in both cases, disease progression and poor clinical condition resulted in decision of euthanasia and necropsy was not authorized.Discussion: Canine lymphoma is often associated with paraneoplastic syndromes, with neuropathy being one of its possible clinical manifestations. In spite of that its pathogenesis remains unclear, with little information in the veterinary literature. Diagnosis is challenging and must be initially based on recognition of neurological clinical signs and lesion localization, as in the reported cases with lesions located on the fifth and seventh cranial nerves. In the patient from the first case, the absence of clinical signs and laboratory abnormalities suggestive of endocrinopathies, associated with neurological signs restricted to the trigeminal nerve, bilaterally, before starting chemotherapy and without the identification of brain lesions in computed tomography, suggested paraneoplastic involvement as the cause of neuropathy. In the second case described, the absence of clinical signs and laboratory abnormalitiess suggestive of endocrinopathies or nutritional deficiencies, associated with neurological signs restricted to the facial and trigeminal cranial nerves, suggested direct or indirect tumour involvement. Both cases showed improvement of neurological clinical signs after chemotherapy which favored the therapeutic diagnosis. Nevertheless, failure to authorize necropsy of patients made it impossible to confirm that peripheral neuropathy is secondary to the remote effect of lymphoma.

EP35 Cryoglobulinaemic vasculitis: an uncommon complication of Sjögren’s syndrome

EP35 Cryoglobulinaemic vasculitis: an uncommon complication of Sjögren’s syndrome

Chapter 19 - Neurolocalization of taste disorders

Neurolocalization of taste disorders requires a knowledge of the functional anatomy involved in mediating taste information from the peripheral mucosal surfaces through numerous peripheral cranial nerves to complex subcortical and cortical brain regions. Our understanding of this functional anatomy has advanced in recent years. Taste is an experience that is both innate and learned, and the "taste" experience involves the integration of information from other sensory modalities, such as olfaction and somatosensation. Normal taste perception is influenced by different neurophysiologic states, which involve endocrine function, emotions, and even attitudes and expectations toward eating. At its core, the normal effective ability to taste is a reflection of the proper function of many organ systems within the body and may be considered a marker for good health. Clinical taste disorders, on the other hand, involve the dysfunction of the normal neural taste pathways and/or aberrant influences on multisensory integration and cortical taste processing. The number of disease processes, which can adversely affect taste, are numerous and quite varied in their presentation. There may be contributory involvement of other organ systems within the body, and the appropriate management of taste disorders often requires a multidisciplinary approach to fully understand the disorder. Depending on the underlying cause, taste disorders can be effectively managed when identified. Treatments may include correcting underlying metabolic disturbances, eliminating infections, changing offending medications, replenishing nutritional deficiencies, operating on structural impairments, calming autoimmune processes, and even stabilizing electrochemical interactions.

Accessory Nerves of the Forehead: A Newly Discovered Frontotemporal Neurovascular Bundle and Its Implications in the Treatment of Frontal Headache, Migraine Surgery, and Cosmetic Temple Filler Injection.

Surgical decompression of peripheral cranial and spinal nerves at several anatomically studied trigger sites has demonstrated significant efficacy in bringing permanent relief to migraine sufferers. In their experience performing frontal nerve decompression on migraine patients, the authors noticed a previously undescribed accessory nerve and vessel in the frontotemporal area, and report its implication in migraine surgery and cosmetic filler injection. A retrospective review of 113 patients who underwent frontal migraine decompression surgery with the senior author at the University of Texas Southwestern Medical Center from July of 2012 to May of 2016 was performed. For the included 76 patients, measurements of this nerve had been taken intraoperatively using high-definition endoscopic assistance, and topographic measurements were correlated with endoscopic location of the nerve. This frontotemporal nerve (FTN) was present in 55 percent, and the bilateral incidence was 57 percent of those. An accompanying vessel was also present in 81 percent of nerve complexes. Both nerve and vessel varied in size. A large vessel was present in 8 percent of all patients, and a medium vessel was present in 20 percent. Consistently, the nerve exited a foramen in the frontal bone on average 3.4 ± 0.47 cm superior to the lateral canthus. The identification and proper avulsion neurectomy of this newly described sensory FTN may lead to better surgical response rate during migraine surgery. In addition, this nerve should be considered during nerve block and botulinum toxin injections in migraine treatment. The existence of the accompanying vessel could have significant implications in the safety of filler and fat injections to this area.

One-year experience in carotid endarterectomy combining general anaesthesia with preserved consciousness and sequential carotid cross-clamping.

Background and aim of the work: We report 1-year single-centre experience in carotid endarterectomy (CEA) combining general anaesthesia with preserved consciousness (GAPC) and standardized carotid sequential cross-clamping, for our protocol effectiveness evaluation in reduction of perioperative stroke, death or cardiologic complications. Methods: We considered all patients who underwent CEA in 2016. All patients underwent superficial cervical plexus block and GAPC with Remifentanil. The surgical technique consisted of common carotid artery (CCA) cross-clamping, carotid bifurcation isolation, external (ECA) and internal carotid artery (ICA) cross-clamping. After CCA cross-clamping, we performed a neurological tolerance test (NTT); this allowed selective shunting only for positive NTT. Primary end-points were: transient ischemic attack (TIA)/stroke, myocardial infarction, death in perioperative period. Secondary end-points were: carotid shunting, peripheral cranial nerves injuries (PCNI), GAPC intolerance, other complications, reintervention in perioperative period, length of hospital stay. Results: 104 consecutive patients underwent CEA with this protocol in the considered period. Twenty-seven (25.9%) patients were symptomatic. Mean clamping time was 48±13.5 minutes. Five cases (4.8%) requested internal carotid artery shunting. No TIA/stroke, myocardial infarction or death were recorded in the perioperative period. PCNI were observed in 19 cases (18.2%) in the immediate post-operative period; 16 of them (84.2%) showed complete or partial resolution at discharge. Only one patient (0.9%) showed GAPC intolerance. No other complication occurred. Three patients (2.9%) underwent reintervention for neck haematoma drainage. Mean hospital stay were 3±0.9 days. Conclusions: GAPC associated with sequential carotid cross-clamping appeared to be safe and effective in prevention of major neurological and cardiologic complications during CEA. (www.actabiomedica.it)

Lithium: one drug, five complications

BackgroundLithium poisoning could trigger multiple complications. We report the case of a lithium poisoning with five complications that are described for the first time together.Case reportA 60-year-old woman was admitted in our intensive care unit for altered consciousness. Severe lithium intoxication was diagnosed (lithium plasmatic level 8.21 mmol/l) associated with acute oliguric kidney failure. Continuous renal replacement therapy was started immediately. Orotracheal intubation was quickly required because of status epilepticus. Medullary aplasia happened 48 h after the patient was intubated. Infectious and immunological causes were ruled out and lithium poisoning was considered as the most likely etiology. Iterative blood and platelet transfusion were required. Severe polyneuropathy was diagnosed on the 5th day after admission. The patient showed a peripheral tetraparesia and cranial nerve failure while lithium plasmatic level had decreased to a therapeutic level. Conversely, urine output increased and hypernatremia promptly occurred, which led to diabetes insipidus diagnosis. Neuropathy decreased in 72 h and the patient was definitely extubated by the 11th day. Hematologic disturbances decreased and no blood transfusion would be required after the 8th day. The patient would keep sequellas of the poisoning. Thin motricity would still be altered and polyuria would remain. Diffuse alopecia was promptly observed, with no iron deficiency or thyroid disturbance.ConclusionIn addition to presenting this case report, we herein discuss the drug causality, the consequences, and the plausible pathophysiology of these five situations.

Palsy – Treatment Efficacy by Drugs and Interferential Current Therapy

Bell's palsy also term idiopathic facial palsy has uncertain etiology. Controversy in management issue makes “Bell's palsy” a novel disorder. Although majority of patients regain their normal or near normal facial motor function, certain percentage of sufferers shows incomplete motor function recovery of peripheral VII cranial nerve with or without troublesome synkinesis. At this context, a randomized clinical trial was made to see the efficacy of interferential current along with medical management for therapeutic benefit and to prevent long term sequallae. Some other important issue like natural history, reactivation of HSV – Type 1 viral etiology, medical, surgical and acupuncture treatment were reviewed.

Relapsing peripheral facial palsy: An unusual early sign of Friedreich ataxia

A 4-year-old child presented with peripheral left facial palsy. Neurological examination was normal except for deep tendon areflexia in the lower limbs. Serologic evaluation and cerebral magnetic resonance imaging to rule out post-infectious causes were normal. Electroneurography (ENG) showed absent sensory action potentials. After 15 days, the patient experienced a relapse of peripheral left facial palsy; ENG was unchanged, and somatosensory evoked potentials showed posterior column involvement. Genetic analysis demonstrated GAA repeat expansion on both alleles (860 and 900 GAA triplets) of the frataxin gene, and the child was diagnosed with Friedreich ataxia. Neurological findings at the last examination, performed at 7 years of age, were unchanged except for mild bilateral pes cavus. Peripheral seventh cranial nerve palsy could be an early and unusual sign of central nervous system degeneration and axonal sensory neuropathy. Its occurrence in this patient provides further evidence that Friedreich ataxia may have a varied clinical presentation at onset. In accordance with other studies, we believe that the size of both GAA expansions affect the age at onset of the disease, despite atypical phenotype.

Visualization of the Peripheral Branches of the Mandibular Division of the Trigeminal Nerve on 3D Double-Echo Steady-State with Water Excitation Sequence

Although visualization of the extracranial branches of the cranial nerves has improved with advances in MR imaging, only limited studies have assessed the detection of extracranial branches of the mandibular nerve (V3). We investigated the detectability of the branches of V3 on a 3D double-echo steady-state with water excitation sequence. We retrospectively evaluated the detectability of the 6 branches of the V3, the masseteric, buccal, auriculotemporal, lingual, inferior alveolar, and mylohyoid nerves, by using a 5-point scale (4, excellent; 3, good; 2, fair; 1, poor; and 0, none) in 86 consecutive patients who underwent MR imaging with the 3D double-echo steady-state with water excitation sequence. Weighted κ analysis was used to calculate interobserver variability among the 3 readers. The detection of the lingual and inferior alveolar nerves was the most successful, with excellent average scores of 3.80 and 3.99, respectively. The detection of the masseteric, the buccal, and the auriculotemporal nerves was good, with average scores of 3.31, 2.67, and 3.11, respectively. The mylohyoid nerve was difficult to detect with poor average scores of 0.62. All nerves had excellent interobserver variability across the 3 readers (average weighted κ value, 0.95-1.00). The 3D double-echo steady-state with water excitation sequence demonstrated excellent visualization of the extracranial branches of V3 in most patients. The 3D double-echo steady-state with water excitation sequence has the potential for diagnosing V3 pathologies and preoperatively identifying peripheral cranial nerves to prevent surgical complications.

Clinical Features of and Treatment Outcome of Neurolymphomatosis: Single Institutional Experience over 7 Years

Abstract Introduction: Neurolymphomatosis (NL) is an extremely rare neurological manifestation of non-Hodgkin lymphoma (NHL) in which peripheral nerve infiltration of lymphoma cells is a dominant feature both clinically and pathologically. Previously, we reported a high frequency of NL as a relapse disease of intravascular large B cell lymphoma (IVL), although NL could present as an initial disease as well as relapsed disease in other types of NHL. In addition, the clinical features and treatment outcomes of NL are largely unknown. However, the recent increase in use of PET/CT in lymphoma has facilitated the diagnosis of NL. Here, we report our experience with NL at our hospital over the period from January 2006 to July 2014. Methods: We reviewed the clinical records at the Hematology/Oncology Department of Kameda Medical Center. The diagnosis of NL required: 1) clinical symptoms and neurological examination findings related to the cranial or spinal nerves; and 2) histological confirmation of malignant lymphoma cells within the peripheral nerve, nerve root/plexus, or cranial nerve; or 3) CT/MRI demonstration of nerve enhancement and/or enlargement of peripheral nerve(s) or nerve root that were also demonstrated by the accumulation of FDG by FDG-PET/CT. Patients with stomach limited mucosa-associated lymphoid tissue (MALT) lymphoma and leukemic infiltration of peripheral nerve due to acute leukemia were excluded from the study. Results: Over the past 7 years, there were 514 patients diagnosed with NHL. Among them, we identified 9 patients (1.8%) diagnosed as having NL. The patients consisted of 2 men and 7 women with a median age of 72 years (range: 63 – 83 years). All 9 patients were histologically diagnosed as a diffuse large B-cell lymphoma (DLBCL). NL occurred as part of the presenting disease in 3 patients and as a relapse disease in the remaining 6 patients. 4 NL patients presented as a relapse disease of IVL, 2 as a relapse disease of nodal DLBCL, and 3 as a concomitant extranodal DLBCL (stomach, ileum, and uterus). CD5 was positive in 7 cases (78%). Diagnosis of NL was made by neurological findings, enlargement and enhancement of affected cranial or peripheral nerves by MRI, and FDG-uptake of affected nerve demonstrated by PET/CT in all patients. Autopsy also confirmed the lymphoma infiltration in 1 patient. The affected nerves included the lumbosacral nerve (5 patients), brachial plexus (2 patients), peroneal nerve (1 patients), cranial nerves (4 patients), especially oculomotor nerve (2 patients), trigeminal nerve (2 patients). Cerebrospinal fluid cytology was positive in 4 cases (44%). All 9 patients received a treatment regimen including high-dose methotrexate (MTX) in addition to rituximab containing systemic chemotherapy. Six patients received involved nerve irradiation, 4 patients at relapse and 2 at presentation. Neurological symptoms of the all patients responded promptly. Six patients subsequently developed CNS involvement despite the prophylactic use of high-does MTX. Six patients died due to progressive NL with a median of 11.3 months after NL development. Three patients are still alive 8, 9, and 92 months from the diagnosis. Two patients received autologous stem cell transplantation (auto-SCT), one survived for more than 7 years but the other relapsed 4 months after auto-SCT and being treated with radiation and chemotherapy. Conclusions: NL occurs in a minority of patients (1.8%) and can present in diverse ways, both at initial diagnosis of lymphoma or after treatment. All of them were DLBCL and 78% were CD5-positive. IVL is a most common type of lymphoma subtype in which develop NL. Contemporary imaging techniques including MRI and PET/CT, can often detect relevant neural involvement. Prognosis remains poor once patient developed NL despite the use of high-dose MTX and rituximab containing aggressive chemotherapy included auto-SCT. Only involved nerve irradiation was effective for the relief of neurologic symptoms. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Videofluoroscopy-Guided Balloon Dilatation for the Opening Dysfunction of Upper Esophageal Sphincter by Postoperative Vagus Nerve Injury: A Report on Two Cases

Dysphagia secondary to peripheral cranial nerve injury originates from weak and uncoordinated contraction-relaxation of cricopharyngeal muscle. We report on two patients who suffered vagus nerve injury during surgery and showed sudden dysphagia by opening dysfunction of upper esophageal sphincter (UES). Videofluoroscopy-guided balloon dilatation of UES was performed. We confirmed an early improvement of the opening dysfunctions of UES, although other neurologic symptoms persisted. While we did not have a proper comparison of cases, the videofluoroscopy-guided balloon dilatation of UES is thought to be helpful for the early recovery of dysphagia caused by postoperative vagus nerve injury.

Ongoing activity of Toscana virus genotype A and West Nile virus lineage 1 strains in Turkey: a clinical and field survey.

Toscana virus (TOSV), West Nile virus (WNV) and tickborne encephalitis virus (TBEV) are among major viral pathogens causing febrile disease and meningitis/encephalitis. The impact of these viruses was investigated at a referral centre in Ankara Province, Central Anatolia in 2012, where previous reports suggested virus circulation but with scarce information on clinical cases and vector activity. Serum and/or cerebrospinal fluid samples from 94 individuals were evaluated, in addition to field-collected arthropod specimens that included 767 sandflies and 239 mosquitoes. Viral nucleic acids in clinical samples and arthropods were sought via specific and generic nested/real-time PCRs, and antibody responses in clinical samples were investigated via commercial indirect immunofluorescence tests (IIFTs) and virus neutralization. A WNV antigen assay was also employed for mosquitoes. WNV neuroinvasive disease has been identified in a 63-year-old male via RNA detection, and the WNV strain was characterized as lineage 1. TOSV infections were diagnosed in six individuals (6.3%) via RNA or IgM detection. Partial sequences in a 23-year-old female, presented with fever and transient pancytopenia, were characterized as TOSV genotype A. Febrile disease with arthralgia and/or peripheral cranial nerve involvement was noted in cases with TOSV infections. Previous WNV and TOSV exposures have been observed in 5.3% and 2.1% of the subjects, respectively. No confirmed TBEV exposure could be identified. Morphological identification of the field-collected mosquitoes revealed Culex pipiens sensu lato (74.4%), Anopheles maculipennis (20.9%), An. claviger (2.1%) and others. Sandfly species were determined as Phlebotomus papatasi (36.2%), P. halepensis (27.3%), P. major s. l. (19.3%), P. sergenti (8.9%), P. perfiliewi (4.4%), P. simici (2.6%) and others. Viral infections in arthropods could not be demonstrated. TOSV genotype A and WNV lineage 1 activity have been demonstrated as well as serologically proven exposure in patients. Presence of sandfly and mosquito species capable of virus transmission has also been revealed.

Ocular myasthenia gravis

To review ocular myasthenia gravis (OMG), a localized form of myasthenia gravis clinically involving only the extraocular, levator palpebrae superioris, and orbicularis oculi muscles. Ocular manifestations can masquerade as a variety of ocular motility disorders, including central nervous system disorders and peripheral cranial nerve palsies. While sparing the pupils, the diagnosis and management can be challenging. Because several diagnostic and treatment options are available for OMG, clinicians must decide the sequence and combination based on the level of disease activity and patient disability.

Presentation of Bilateral Peripheral Seventh Cranial Nerve Palsy in an HIV Patient

Neurological manifestations in patients infected with human immunodeficiency virus can significantly increase overall morbidity and mortality. These complications are neither limited to a specific location in the nervous system nor a focal time period in the disease's progression. A literature review yielded several cases of peripheral facial palsy associated with HIV seropositivity, but few cases have been reported where the patient had bilateral peripheral facial palsy. In this paper, we present a patient with bilateral peripheral facial palsy and aseptic meningitis in the context of newly diagnosed HIV.

Central mechanisms of cranial nerve stimulation for epilepsy

Stimulation of peripheral cranial nerves has been shown to exert anticonvulsant effects in animal models as well as in human patients. Specifically, stimulation of both the trigeminal and vagus nerves has been shown in multiple clinical trials to be anticonvulsant, and stimulation of these nerves at therapeutic levels does not cause pain or negatively affect brain function. However, the neuronal mechanisms by which such stimulation exerts therapeutic effects are not well understood. In this review, the possible locations of action for trigeminal nerve stimulation (TNS) and vagus nerve stimulation (VNS) are explored. Additionally, the multiple time scales on which TNS and VNS function are discussed.

The history of facial palsy and spasm

Although Sir Charles Bell was the first to provide the anatomic basis for the condition that bears his name, in recent years researchers have shown that other European physicians provided earlier clinical descriptions of peripheral cranial nerve 7 palsy. In this article, we describe the history of facial distortion by Greek, Roman, and Persian physicians, culminating in Razi's detailed description in al-Hawi. Razi distinguished facial muscle spasm from paralysis, distinguished central from peripheral lesions, gave the earliest description of loss of forehead wrinkling, and gave the earliest known description of bilateral facial palsy. In doing so, he accurately described the clinical hallmarks of a condition that we recognize as Bell palsy.

A monofocal pontine lesion

The patient was admitted for confusion and a resultant tracheal laceration sustained after her fall which was complicated with subcutaneous emphysema and infection. Diagnostic studies revealed normal serum electrolytes, cerebrospinal fluid study, vitamin B12 level, and tests for rheumatological diseases. Chronic alcoholism was felt to be the cause of the central pontine myelinolysis (CPM). The patient improved significantly with antibiotics and surgical tracheal repair and was discharged with minimal memory residual deficits. Repeat MRI of the brain more than 6 months later showed decreased but persistent hyperintensity in the midpons (Fig. 1). CPM is most commonly associated with: alcoholism, 39.4% of patients; rapid reversal of hyponatremia, 21.5%; and liver transplantation, 17.5%. Prognosis for CPM is reported to be invariably fatal but patients with complete recovery with mild impairment have been seen. Three subtypes of these brain demyelinating diseases are known: (i) CPM, confined to the pons; (ii) extrapontine myelinolysis (EPM); and (iii) osmotic demyelinating syndrome (ODS), in which CPM and EPM are both present. Adult pontine gliomas are rare tumors that usually present clinically with gait disturbance, headaches, weakness of limbs, and cranial nerve involvement. MRI findings include a non-enhancing diffusely infiltrative mass, enhancing localized mass, and isolated tectal tumor. The absence of these findings in our patient made the diagnosis of a pontine glioma unlikely. Pontine infarctions usually present with findings that may include ipsilateral peripheral cranial nerve palsies, contralateral movement disorders, sensory disturbances, and pure motor hemiparesis or hemiplegia. MRI findings typically include a well-demarcated hyperintensity in the pons on T2-weighted MRI with a corresponding hypointensity on T1-weighted MRI. Multiple sclerosis is a chronic, persistent inflammatory–demyelinating disease of the central nervous system that typically presents as an acute clinically isolated syndrome attributable to a monofocal or multifocal demyelinating lesion,