CRANIAL NEUROPATHIES I, V, AND VII–XII

2014 ◽  
pp. 680-709
Keyword(s):  
Cranial Neuropathies

scholarly journals Clival metastasis from a gastrointestinal adenocarcinoma causing multiple cranial neuropathies

2017 ◽  
pp. bcr-2017-222725
Author(s):  
Charlotte Lee ◽  
Jesse M Thon ◽  
Amar Dhand
Keyword(s):  
Cranial Neuropathies

scholarly journals Confounding case of seromucinous hamartoma

2021 ◽  
Vol 14 (3) ◽  
pp. e240460
Author(s):  
Neal Rajan Godse ◽  
Giuseppe Vittorio Staltari ◽  
Katherine Doeden ◽  
Grant Shale Gillman
Keyword(s):  
Myasthenia Gravis ◽  
Vocal Fold ◽  
Cranial Nerves ◽  
Vocal Fold Paralysis ◽  
Seromucinous Hamartoma ◽  
Cranial Neuropathies ◽  
Receptor Antibodies ◽  
Bony Erosion ◽  
Ct And Mri ◽  
Anti Acetylcholine

A 67-year-old man presented with progressive diplopia. On evaluation, he was noted to have bilateral palsies of cranial nerves III, IV and VI as well as a unilateral right true vocal fold paralysis. CT and MRI studies demonstrated a T2-bright left ethmoid mass with no evidence of bony erosion. Direct visualisation demonstrated a polypoid appearing mass of the left sphenoethmoid recess. Operative biopsy was pursued with final pathology demonstrating benign seromucinous hamartoma. Subsequent blood work demonstrated high titres of anti-acetylcholine receptor antibodies consistent with myasthenia gravis. The patient was started on pyridostigmine with improvement in his ocular cranial neuropathies.

scholarly journals DIPG-72. LONG-TERM SURVIVAL OF A CLASSIC DIFFUSE INTRINSIC PONTINE GLIOMA TREATED WITH NIMOTUZUMAB

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii301-iii301
Author(s):  
Sidnei Epelman ◽  
Vijay Ramaswamy ◽  
Ethel Gorender ◽  
Luis Henrique Sakamoto
Keyword(s):  
Diffuse Intrinsic Pontine Glioma ◽  
Pontine Glioma ◽  
Tumor Biopsy ◽  
Term Survival ◽  
Long Term Survival ◽  
Good School ◽  
Cranial Mri ◽  
Cranial Neuropathies ◽  
Image Assessment

Abstract BACKGROUND Long-term survival in diffuse intrinsic pontine glioma is rare, and typically associated with atypical imaging and/or atypical clinical course. Although most patients harbor hotspot mutations in H3.1/3-K27M, a proportion of patients have alternate mutations, despite a typical clinicoradiological course. Herein we describe a long-term survivor with a classical presentation, treated with nimotuzumab, highlighting the challenges associated with such cases. CASE REPORT: A 5 year old male, diagnose in 2012 with a 10 day history multiple cranial neuropathies and a right hemiparesis. Cranial MRI revealed a poorly delimited diffuse pontine tumor and secondary hydrocephalus. Tumor biopsy was not performed due to the classic clinical presentation, and he received 54Gy/30 of radiation plus concomitant weekly nimotuzumab 150mg/m2. Initial tumor dimensions were 43x31x28mm. Nimotuzumab 150mg/m2 was continued every 2 weeks. Image assessment at week 12 of treatment revealed 16.9% volume increase, 4 weeks after radiotherapy completion. Nevertheless, subsequent neuroimaging at 24th, 36th, 60th, 96th and 108th weeks of nimotuzumab therapy showed a sustained and progressive tumor cytoreduction of 47.5%, 59%, 62.2%, 63.8% and 67%, respectively, when compared with post-radiotherapy dimensions. Currently, the patient is 13y old, good school performance, no neurologic disabilities. The last MRI at 394 weeks of nimotuzumab revealed dimensions of 21x19x14mm which corresponds to 70% of reduction compared with initial volume. CONCLUSIONS Our case of progressive cytoreduction over two years of a classic DIPG, diagnosed in the era prior to the discovery of the K27M mutation, highlights the challenges associated with long-term survival of this devastating entity.

Cranial Neuropathies II, III, IV, and VI

2020 ◽  
pp. 693-716
Author(s):  
Tanyatuth Padungkiatsagul ◽  
Heather E. Moss
Keyword(s):  
Cranial Neuropathies

scholarly journals Cranial neuropathies in sarcoidosis

2015 ◽  
Vol 5 (1) ◽  
pp. 16 ◽  
Author(s):  
Hussam A Yacoub
Keyword(s):  
Cranial Neuropathies

A case of nonsystemic vasculitic neuropathy presenting with multiple cranial neuropathies

2012 ◽  
Vol 60 (6) ◽  
pp. 653 ◽  
Author(s):  
JeeYoung Kim ◽  
DongSun Kim ◽  
BonDae Ku ◽  
HyunJung Han ◽  
Heasoo Koo
Keyword(s):  
Vasculitic Neuropathy ◽  
Cranial Neuropathies ◽  
Nonsystemic Vasculitic Neuropathy

Invasive rhino-orbito-cerebral aspergillosis presenting as multiple cranial neuropathies – A case report

2021 ◽  
Vol 429 ◽  
pp. 118956
Author(s):  
Miguel Miranda ◽  
Vera Montes ◽  
Sandra Sousa ◽  
Fernando Pita ◽  
Cátia Carmona
Keyword(s):  
Case Report ◽  
Cranial Neuropathies

Approach to Facial Weakness

2021 ◽  
Vol 41 (06) ◽  
pp. 673-685
Author(s):  
Yujie Wang ◽  
Camilo Diaz Cruz ◽  
Barney J. Stern
Keyword(s):  
Facial Palsy ◽  
Treatment Options ◽  
Cranial Neuropathy ◽  
Facial Weakness ◽  
Ramsay Hunt Syndrome ◽  
Corneal Injury ◽  
Diagnostic Measures ◽  
Fluid Analysis ◽  
Hunt Syndrome ◽  
Cranial Neuropathies

AbstractFacial palsy is a common neurologic concern and is the most common cranial neuropathy. The facial nerve contains motor, parasympathetic, and special sensory functions. The most common form of facial palsy is idiopathic (Bell's palsy). A classic presentation requires no further diagnostic measures, and generally improves with a course of corticosteroid and antiviral therapy. If the presentation is atypical, or concerning features are present, additional studies such as brain imaging and cerebrospinal fluid analysis may be indicated. Many conditions may present with facial weakness, either in isolation or with other neurologic signs (e.g., multiple cranial neuropathies). The most important ones to recognize include infections (Ramsay-Hunt syndrome associated with herpes zoster oticus, Lyme neuroborreliosis, and complications of otitis media and mastoiditis), inflammatory (demyelination, sarcoidosis, Miller–Fisher variant of Guillain–Barré syndrome), and neoplastic. No matter the cause, individuals may be at risk for corneal injury, and, if so, should have appropriate eye protection. Synkinesis may be a bothersome residual phenomenon in some individuals, but it has a variety of treatment options including neuromuscular re-education and rehabilitation, botulinum toxin chemodenervation, and surgical intervention.

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