Petrous apicitis presenting with Horner’s syndrome

Ibrikji, Sidonie; Rizk, Nesrine

doi:10.1007/s13760-021-01692-4

Cited by 2 publications

(1 citation statement)

References 8 publications

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“…A recent classification proposal has divided the diagnostic categories of GS into three groups: classic presentation with evidence of PA, abducens nerve palsy, OM and trigeminal nerve pain; incomplete presentation with evidence of PA, abducens nerve palsy and OM or trigeminal nerve pain; mimic presentation without evidence of PA and abducens nerve palsy and OM or trigeminal nerve pain [20]. The possible spread infection to nearby structures can generate heterogeneous complications as meningitis, intracranial abscess, involvement of IX, X, XI cranial nerves (Vernet's syndrome) [21], prevertebral/parapharyngeal abscess, palsy, ipsilateral septic cavernous sinus thrombosis, cerebral venous sinus thrombosis, infectious arteritis of the internal carotid artery, carotid canal bone erosion, involvement of the jugular foramen and extension to sympathetic plexus with Horner's syndrome [1,2,11,[22][23][24]. The wide variety of clinical presentation can represent a challenge for physicians and lead to a wrong diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Refractory Pseudomonas Osteomyelitis of the Skull Base With Gradenigo’s Syndrome: Early Dysphagia and Late Abducens Nerve Palsy

Mammarella,

Loperfido,

Velletrani

et al. 2024

J Med Cases

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Gradenigo's syndrome (GS) is a rare entity characterized by otitis media, pain in the trigeminal nerve distribution and abducens nerve palsy. The classic triad is uncommon, making the diagnostic workup challenging. Specifically, the diagnostic approach includes medical history, a complete otorhinolaryngological examination, a pure-tone audiogram and radiological investigation such as contrast-enhanced computed tomography scan and magnetic resonance imaging of head and neck. Broad-spectrum antibiotics are the first-line treatment, such as intravenous (IV) ceftriaxone and IV metronidazole. Here, we present the case of a 71-year-old man with a previous history of otitis media and poorly controlled type 2 diabetes mellitus. He presented to our attention with facial pain, left hemilarynx paralysis, dysphagia and otorrhea. The patient was treated with broad-spectrum antibiotics without any clinical improvement. Imaging evaluations demonstrated the presence of wide and poorly defined pathological material with epicenter in the masticatory space, involving all nearby structures. The patient underwent multiple biopsies without obtaining a definitive tissue diagnosis of neoplasia. After 2 months, the patient developed delayed VI cranial nerve palsy, providing evidence of GS. Although incomplete, GS has been described in the literature; however, none of the cases exhibited a latent abducent deficit. To the best of our knowledge, this is the only case with a delayed onset of abducens nerve palsy.

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Section: Discussionmentioning

confidence: 99%

Refractory Pseudomonas Osteomyelitis of the Skull Base With Gradenigo’s Syndrome: Early Dysphagia and Late Abducens Nerve Palsy

Mammarella,

Loperfido,

Velletrani

et al. 2024

J Med Cases

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Gorner syndrome as a sign of dyscirculatory disorders

Miroshnikova,

Krivonozhkina

2024

Bulletin of Neurology, Psychiatry and Neurosurgery

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The article discusses the issues of the normal anatomy of the autonomic innervation of the eye muscles, mainly its sympathetic part. The symptoms included in the Claude Bernard Horner's syndrome, which occurs when the sympathetic pupillomotor pathway is affected, are considered. The causes of this syndrome are numerous. The classification of acquired conditions the clinical picture of which involves Horner syndrome is given. Three classes of etiological processes are distinguished: central (suprasegmental and segmental), peripheral, and idiopathic. Nosological components are listed for each of these. The complexity of the topographic anatomy of the sympathetic pathways innervating the eye muscles leads to significant difficulties in diagnosing the level of their lesion. Pathological processes affecting the peripheral part of the sympathetic chain are detected much faster, as the causes that provoked the development of Horner syndrome are often more obvious and diagnostically accessible. Cases of Horner syndrome of central genesis are significantly more difficult in diagnostic terms. The ar ticle discusses additional symptoms that form the clinical picture for stem strokes, tumors of the hypothalamic-pituitary region and brain stem, multiple sclerosis, and various diseases of the spinal cord, where the Claude Bernard Horner's syndrome is part of the clinical picture. In such cases, the analysis of neurological symptoms provides the basis for niveau diagnosis. The most difficult situations are when the only reason for the patient's visit and the objective component of the neurological status is just a triad of symptoms: miosis, partial ptosis, and enophthalmos. The paper presents an example of a similar case from clinical practice, when a patient with an acutely developed isolated left-sided symptom complex, including miosis, ptosis, and enophthalmos, had a focus of lacunar strok e in the lef t thalamo-hypothalamic region.

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Petrous apicitis presenting with Horner’s syndrome

Cited by 2 publications

References 8 publications

Refractory Pseudomonas Osteomyelitis of the Skull Base With Gradenigo’s Syndrome: Early Dysphagia and Late Abducens Nerve Palsy

Refractory Pseudomonas Osteomyelitis of the Skull Base With Gradenigo’s Syndrome: Early Dysphagia and Late Abducens Nerve Palsy

Gorner syndrome as a sign of dyscirculatory disorders

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