In the routine evaluation of patients with facial pain, the clinician will inevitably be confronted with secondary pathology of the trigeminal nerves and nuclei. The appearance of numbness, even when pain continues to be the most pressing complaint, necessitates clinical assessment of the integrity of all aspects of the trigeminal pathways, which may also include neurophysiologic, radiographic, and laboratory evaluation.
This article reports a case of secondary short-lasting unilateral neuralgiform headache with conjunctival injection and tearing following head and neck trauma due to a violent assault. Following the incident, the patient began experiencing 4 to 30 shooting/sharp pain attacks per day in the left anterior temporal and supraorbital areas, with an intensity of 10/10 on a numeric rating scale. Each attack lasted between 10 and 60 seconds. These attacks were accompanied by ipsilateral conjunctival injection, tearing, ptosis of the left eye, blurry vision, and occasional rhinorrhea. Significant improvements in sleep, autonomic symptoms, and pain were observed with a combination of melatonin 10 mg per day, gabapentin 300 mg twice daily, physical therapy, and psychotherapy. This case highlights the relevance of a multidisciplinary approach in the treatment of challenging cases when there is evidence of more than one contributing factor, with the aim of reducing pain and improving the patient's quality of life.
We describe the case of a 59-year-old woman who presented with progressive bilateral vestibular hypofunction and who was found to have bilateral granulomatous mass lesions of the mesial temporal lobe. Initially, her condition stabilized neurologically with corticosteroids, but a diagnosis of neurosarcoidosis was delayed because of the unusual presentation and persistently normal chest imaging results and serum angiotensin-converting enzyme (ACE) levels. Approximately 1 year after her initial presentation, the patient died of complications of a myocardial infarction and pulmonary embolism. Sarcoidosis should be considered in the differential diagnosis of idiopathic bilateral vestibular hypofunction even if the chest imaging and serum ACE levels are normal, particularly when there is evidence of a multisystem process.
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