scholarly journals Wallenberg syndrome with ipsilateral upper motor neuron facial palsy: A rare manifestation

2022 ◽  
Vol 10 (1) ◽  
pp. 48
Author(s):  
Pallav Jain ◽  
Vijay Sardana
2011 ◽  
Vol 17 (2) ◽  
pp. 58
Author(s):  
M Venugopal ◽  
R Suma ◽  
Sheeja Rajan ◽  
Subin Thomas

2011 ◽  
Vol 2011 (jan29 1) ◽  
pp. bcr1220103564-bcr1220103564
Author(s):  
D. K. Gupta ◽  
V. Atam ◽  
S. C. Chaudhary

1991 ◽  
Vol 105 (7) ◽  
pp. 568-570 ◽  
Author(s):  
R. C. Nayar ◽  
I. Garg ◽  
J. J. Alapatt

AbstractA case of malakoplakia, of the temporal bone in a nine-month-old male child is reported.The lesion presented as an aural polyp, associated with a lower motor neuron facial palsy. On exploration, the granuloma was noted to involve the temporal bone, eroding the bony labyrinth. It was successfully treated with surgical debridement, and antibiotics. A review of the relevant literature is presented.


Author(s):  
Puspraj Awasthi ◽  
Sudeep K. C. ◽  
Prasanna Samynathan ◽  
Arun Bansal

2015 ◽  
Vol 2015 (apr28 1) ◽  
pp. bcr2014206938-bcr2014206938 ◽  
Author(s):  
R. V. Ramdasi ◽  
V. Rangarajan ◽  
A. Mahore

2017 ◽  
Vol 4 (39) ◽  
pp. 2360-2363
Author(s):  
Souvagini Acharya ◽  
Nirupama Pati ◽  
Lakshmana Kumar Panda

2021 ◽  
Vol 7 (2) ◽  
pp. 107-109
Author(s):  
Sajid Ali Shah ◽  
Sohail Shahzad

A 5 years old child with pertussis reported to us with a unique complication not mentioned in the literature. He was thoroughly examined and investigated to find out cause for his lower motor neuron (LMN) facial palsy but purtussis seemed to be the sole reason. With treatment of purtussis the patient showed marked improvement of neurological deficit. Bangladesh Journal of Infectious Diseases 2020;7(2):107-109


Author(s):  
Vykuntaraju K. Gowda ◽  
Anusha Raj ◽  
Dhananjaya K Vamyanmane ◽  
Vani H. Nagarajappa ◽  
Sahana M. Srinivas ◽  
...  

AbstractHyperphosphatemic familial tumoral calcinosis (HFTC) presents with varied neurological manifestations that have been reported in the literature like facial palsy, vision and hearing impairment, stroke, and headache. In this article, we reported a 12-year-old girl child patient with recurrent facial weakness with bilateral hearing impairment and multiple ulcerative lesions on lower limbs and elbows. On examination, she had lower motor neuron (LMN) facial palsy with conductive hearing loss. The investigations showed hyperphosphatemia (9.3 mg/dL) with normal serum calcium (10.4 mg/dL), alkaline phosphatase (147.9 U/L), parathyroid hormone (23.12 pg/mL), and renal function tests. Elevated serum calcium and phosphorus product (96.72 mg2/mL2) and elevated renal tubular reabsorption of phosphate (TMPxGFR) value (9.16) were noted. Skeletal survey showed hyperostosis in the long bone diaphysis, vertebrae, ribs, pelvic bone, skull, and facial bones with narrowing of cranial ostium, characteristically without any peri-articular soft tissue calcifications. An angiogram showed multiple intravascular calcifications. She was managed with a low-phosphate diet, sevelamer, niacinamide, acetazolamide, sucroferric oxyhydroxide to lower serum phosphate level, and topical sodium thiosulfate ectopic cutaneous calcification. Exome sequencing showed novel homozygous inframe deletion of ACG in FGF23 gene exon 3 at c.374_376 delins position (p. Asp125del) in the proband and a mutation in the heterozygous state in the mother and elder sibling, thus confirming a molecular diagnosis of HFTC. Our case had a unique neurological presentation of recurrent bilateral lower motor nerve facial palsy, hearing loss, multiple ectopic cutaneous calcifications without peri-articular deposits, multiple intravascular, intracranial, and vertebral endplate calcification, which has not been reported earlier. The proband showed a novel pathogenic variant suggesting an expanding phenotype of HFTC.


Author(s):  
Jeffrey A. Cohen ◽  
Justin J. Mowchun ◽  
Victoria H. Lawson ◽  
Nathaniel M. Robbins

Facial neuropathy is most commonly seen as an idiopathic unilateral palsy known as Bell’s palsy. Generally, acute onset of typical lower motor neuron facial weakness that is not associated with other atypical or suspicious features, remains unilateral, and recovers completely requires no further workup. A recurrent or bilateral peripheral facial palsy makes an idiopathic cause less likely and prompts a more in-depth workup. The appropriate work-up of unilateral or bilateral facial palsy guided by the presence or absence of associated clinical findings is discussed. The major differentials for bilateral facial paresis include brainstem (especially pontine and prepontine) tumors, Lyme disease (especially in endemic areas), basal menigitides, Guillain-Barre syndrome, and sarcoidosis.


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