Severe hyponatremia and bilateral sequential facial palsy: A case report

Abstract

Facial palsy (FP) is a known consequence of head trauma, manifesting either immediately at the time of injury or with delayed onset, typically occurring 2 days or more post-trauma. Unilateral FP is the more common presentation and is often attributed to partial or complete transection of facial nerves or delayed onset edema. Conversely, bilateral facial palsy is a rare occurrence, reported in only a small number of cases, accounting for approximately 3% of patients presenting with bilateral weakness. In this report, we present the case of a previously healthy 28-year-old female who suffered a closed head injury during the Beirut Port Blast. Four days following the incident, the patient exhibited right-sided peripheral FP, which was consistent with a right temporal bone fracture. Subsequently, on the fifth day, the right-sided FP worsened, accompanied by the development of new FP on the left side, characterized by sparing of the frontal region, indicating a central origin for the left-sided FP. Laboratory investigations revealed severe hypovolemic hyponatremia with a sodium level of 105 mmol/L. As isotonic saline fluid replacement was initiated, there was progressive improvement in the left-sided FP. The right-sided palsy also resolved gradually with the implementation of facial rehabilitation therapy. It is important to note that severe head trauma, particularly with a concussive injury, can lead to facial paralysis through various mechanisms. Furthermore, severe hyponatremia should be considered a potential cause of central facial palsy, particularly in the presence of bilateral facial involvement. A thorough evaluation is encompassing assessment of palsy patterns, comprehensive imaging studies, and metabolic investigations is crucial for accurate diagnosis and timely intervention, resulting in successful treatment.

Keywords: Facial; Hyponatremia; Isotonic saline; Neurosurgery; Palsy; Sequential symptoms.

Fig. 1

Cranial MRI on First Presentation. (A) left superior frontal gyrus 1 cm hemorrhagic focus, (B) high FLAIR T2 signal involving the posterior aspect of the corpus callosum.

Fig. 2

Cranial CT scan on First Presentation. Black arrow: fractured temporal bone. (A) axial cut, left longitudinal temporal bone fracture, sparing the geniculate ganglion, and facial nerve, (B) coronal cut, right geniculate ganglion involved in the fracture.

Fig. 3

Cranial MRI on Second Presentation. Axial DWI sequences (A, B) and axial DWI (C, D) show extensive diffusion restriction with low ADC signal involving the corpus callosum and the cerebral white matter at the corona radiata bilaterally.