alexa In Cranial Nerves Palsy, Do not Miss Fungal Etiology | Open Access Journals
ISSN: 2329-6895
Journal of Neurological Disorders
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In Cranial Nerves Palsy, Do not Miss Fungal Etiology

Attia TH1* and Saeed MA2
1Pediatric Department, Zagazig University, Egypt
2Tropical Medicine Department, Zagazig University, Egypt
Corresponding Author : Attia TH
Pediatric Department
Zagazig University, Egypt
Tel: +00201276099800
E-mail: tareqhamed@live.com
Received: November 30, 2015 Accepted: December 02, 2015 Published: December 04, 2015
Citation: Attia TH, Saeed MA (2015) Cranial Nerves Deficit Due to Rhino Cerebral Mucormycosis. J Neurol Disord 3:i003. doi: 10.4172/2329-6895.1000i003
Copyright: © 2015 Attia TH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Mucormycosis is a rare opportunistic fungal infection caused by filamentous fungi of order Mucorale. It is characterized by infection and necrosis of host tissue that is resulted from invasion of vasculature by hyphae. The genera most commonly found in human infection is Rhizopus and Mucor [1]. Based on its clinical presentation and anatomic sites invasive mucormycosis is classified into 6 clinical forms: rhino-cerebral, pulmonary, cutaneous, gastro-intestinal, disseminated and uncommon rare form such as endocarditis, peritonitis and renal infection

Keywords
Cranial nerves; Cerebral mucormycosis
Case and Discussion
Mucormycosis is a rare opportunistic fungal infection caused by filamentous fungi of order Mucorale. It is characterized by infection and necrosis of host tissue that is resulted from invasion of vasculature by hyphae. The genera most commonly found in human infection is Rhizopus and Mucor [1]. Based on its clinical presentation and anatomic sites invasive mucormycosis is classified into 6 clinical forms: rhino-cerebral, pulmonary, cutaneous, gastro-intestinal, disseminated and uncommon rare form such as endocarditis, peritonitis and renal infection [2]. The most important risk factors predisposing to mucormycosis include malignant hematological diseases, prolonged and sever neutropenia, poorly controlled diabetes mellitus with or without ketoacidosis, major trauma, prolonged use of corticosteroid and malnutrition [1,3] (Figure 1).
In most cases the infection is rapidly progressive and results in death unless underlying risk factors are corrected and aggressive treatment, with antifungal agents and surgical excision, is initiated [3]. Rhinocerebral mucormycosis (RCM) is the most common and fatal clinical form of mucormycosis which presumed to start with inhalation of spores into paranasal sinuses of susceptible host [1]. Dental care may also precede such an infection by creating a post extraction wound which may be susceptible to fungal infection as seen in our case [4]. Hyperglycemia, usually with an associated metabolic acidosis, is the most common underlying condition [1]. Rhizopus organisms have an enzyme, ketone reductase, which allow them to thrive in high glucose levels, at the same time hyperglycemia may alter the immunologic capability to resist mucormycosis through reduction of leucocytes chemotaxis [5].
We present a case of RCM in a 14 years-old diabetic girl who presented with a 2 weeks history of left facial and periorbital swelling associated with left facial numbness and hypoesthesia in the area supplied by ophthalmic, maxillary and mandibular branches of the fifth cranial nerve (Figure 2).
Also there was left facial palsy. The hall marks of spread of infection beyond the sinuses are tissue necrosis of the palate resulting in palatal eschar, facial swelling, erythema and cyanosis of the facial skin overlying the involved sinuses [6]. Signs of orbital involvement include periorbital edema, proptosis and blindness. Facial numbness is frequent and results from infarction of sensory branches of the fifth cranial nerve [7]. Our patient had left facial numbness and hypoesthesia in the area supplied by ophthalmic, maxillary and mandibular branches of the fifth cranial nerve (Figure 3).
Computed tomography (CT) revealed mucosal thickening of all left paranasal sinuses as well as destruction of the posterior wall of the antrum and retro-antral extension.
Further imaging with magnetic resonance imaging (MRI) also showed involvement of all left paranasal sinuses with retro-orbital extension and there was abscess formation in the anterior maxillary area and left orbital floor (Figure 3) as well as mucosal thickening of the left maxillary antrum with areas of low signal intensity (Figure 4).
There was no involvement of central nervous system. Based on the history, clinical presentation and imaging findings a provisional diagnosis of RCM was considered. Fungal cultures confirmed the clinical diagnosis (Figures 5 and 6).
Treatment of RCM is based on reversal of underlying predisposing factor, prompt initiation of antifungal therapy and surgical debridement of involved tissues [3]. However there was no any recommendation in the literature on the duration of antifungal, extent and timing of appropriate surgical management. Our case was successfully treated with antifungal liposomal amphotericin B and posaconazole, as step-down therapy for 8 months, and minimal surgical debridement.
Conclusion
Mucormycosis should be considered in a predisposed patient who presented with cranial nerves deficits. Although extensive surgical debridement could not be performed, disease regression could be achieved with medical therapy and minimal debridement. We present this case because of the rarity of RCM, calling for prompt initiation of treatment in a suspected case and to present data about therapeutic modality.
References

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