Post-concussive Dizziness: A Review and Clinical Approach to the Patient

Dizziness is a frequent complaint after head trauma. Among patients who suffer a concussion (mild traumatic brain injury or mTBI), dizziness is second only to headache in symptom frequency. The differential diagnosis of post-concussive dizziness (PCD) can be divided into non-vestibular, central vestibular and peripheral vestibular causes with growing recognition that patients frequently exhibit both central and peripheral findings on vestibular testing. Symptoms that traditionally have been ascribed to central vestibular dysfunction may be due to peripheral dysfunction. Further, our ability to test peripheral vestibular function has improved and has allowed us to identify peripheral disorders that in the past would have remained unnoticed. The importance of the identification of the peripheral component in PCD lies in our ability to remedy the peripheral vestibular component to a much greater extent than the central component. Unfortunately, many patients are not adequately evaluated for vestibular disorders until long after the onset of their symptoms. Among the diagnoses seen as causes for PCD are (1) Central vestibular disorders, (2) Benign Paroxysmal Positional Vertigo (BPPV), (3) Labyrinthine dehiscence/perilymph fistula syndrome, (4) labyrinthine concussion, (5) secondary endolymphatic hydrops, (6) Temporal bone fracture, and (7) Malingering (particularly when litigation is pending). These diagnoses are not mutually exclusive and PCD patients frequently exhibit a combination of these disorders. A review of the literature and a general approach to the patient with post-concussive dizziness will be detailed as well as a review of the above-mentioned diagnostic categories.

Complete Facial Paralysis Caused by Stabbing With a Car Key at the Stylomastoid Foramen

Non-iatrogenic traumatic facial paralysis is most common in intratemporal facial nerve injury caused by temporal bone fracture, followed by intraparotid facial nerve branch injury. Facial paralysis caused by injury to the extratemporal trunk of the facial nerve is extremely rare. We present a case of a 60-year-old man suffering from immediate complete left peripheral facial paralysis due to blunt transection of extratemporal trunk of facial nerve by stabbing with a car key. There was a facial nerve defect about 1 cm in length. The great auricular nerve was grafted to repair the facial nerve. Over 12 months, his facial nerve function improved to a House–Brackmann III/VI.

Inner Ear Symptoms Are Prevalent in Patients with High Head Abbreviated Injury Scale Scores after Blunt Head Trauma

<b><i>Introduction:</i></b> The purpose of this article was to determine the prevalence of inner ear symptoms in patients with blunt head trauma and to explore whether the severity of head trauma was associated with the incidence of such symptoms. <b><i>Methods:</i></b> We performed a retrospective review of 56 patients admitted with blunt head trauma who underwent audiovestibular evaluation within 1 month after injury. Two scales were used to measure the severity of trauma; these were the Glasgow Coma Scale (GCS) and the Head Abbreviated Injury Scale (H-AIS). Patients with sensorineural-type hearing loss, or dizziness with nystagmus, were considered to have inner ear symptoms. <b><i>Results:</i></b> About half of all patients (45%) with blunt head trauma showed trauma-related inner ear symptoms. Patients with inner ear symptoms were significantly more likely to have H-AIS scores ≥4 than those without inner ear symptoms (<i>p</i> = 0.004), even without concomitant temporal bone fracture (<i>p</i> &#x3e; 0.05). Also, patients with inner ear symptoms required a statistically significantly longer time (measured from admission) before undergoing their ontological evaluations than did those without such symptoms (<i>p</i> = 0.002), possibly due to prolonged bed rest and use of sedatives. <b><i>Conclusion:</i></b> Thus, detailed history-taking and early evaluation using trauma scales are essential for all patients suffering from severe head trauma. It may be necessary to initiate early treatment of traumatic inner ear diseases.

Static Suspension of the Paralyzed Face Utilizing the Midfacial Corridor: Anatomic Evaluation and Surgical Technique

Introduction Fascia lata and tendon grafts are frequently utilized to support the paralyzed midface and to extend muscular reach in McLaughin style, orthodromic temporalis transfers. The grafts are frequently placed in a deep subcutaneous positioning that can lead to the development of a, bowstring deformity in the cheek. This paper describes insertion of tendon grafts into the midfacial corridor collectively formed by the buccal, submasseteric and superficial temporal spaces. Methods Over a seven-year period, all patients that underwent insertion of facia lata and tendon grafts in the midfacial corridor were included. Demographic information, perioperative variables and clinical outcomes were collected and analyzed. Results A total of 22 patients were included with a mean age of 64.3 years (33–86). There were multiple etiologies for the facial weakness including acoustic neuroma (9.1%), Bell's palsy (13.6%), facial nerve schwannoma (9.1%), temporal bone fracture (4.6%) and malignancy (22.7%). Midfacial corridor grafts were utilized in combination with nerve transfers (V-VII and XII-VII) in nine patients, McLaughin style temporalis transfers in 12 and as a standalone procedure in one individual. During the study period, no patients exhibited a tethering, or concave deformity in the midface. Additionally, no impingement, difficulties with mastication, parotitis or hematoma were encountered. One patient developed a postoperative infection, that was successfully managed. Conclusion Placement of tendon or fascia grafts for static support or tunneling of an orthodromic temporalis transfer through the midfacial corridor can be performed rapidly while providing midfacial support and avoiding the creation of visible cutaneous deformities.

Cranial cerebrospinal fluid leak and intracranial hypotension syndrome – a case report

Spontaneous intracranial hypotension is a rare clinical entity caused in most cases by a cerebrospinal fluid leak occurring at the level of the spinal cord. Cranial dural leaks have been previously reported as a cause of orthostatic headaches but, as opposed to spinal dural leaks, were not associated with other findings characteristic of spontaneous intracranial hypotension. We present the case of a male admitted for severe orthostatic headache. The patient had a history of intermittent postural headaches, dizziness, and symptoms consistent with post-nasal drip, which appeared several years after head trauma. Brain imaging showed signs consistent with intracranial hypotension: bilateral hygromas, subarachnoid hemorrhage, superficial siderosis, diffuse contrast enhancement of the pachymeninges, and superior sagittal sinus engorgement. No spinal leak could be identified by magnetic resonance imaging, and the patient had a rapid remission of symptoms with conservative management. Further work-up identified an old temporal bone fracture which created a route of egress between the posterior fossa and the mastoid cells. Otorhinolaryngology examination showed pulsatile bloody discharge and liquorrhea at the level of the left pharyngeal opening of the Eustachian tube. The orthostatic character of the headache, as well as the brain imaging findings, were consistent with intracranial hypotension syndrome caused by a cranial dural leak. Clinical signs and imaging findings consistent with the diagnosis of apparently “spontaneous” intracranial hypotension should prompt the search for a cranial dural leak if a spinal leak is not identified.