Trigeminal neuralgic-type pain and vascular-type headache due to gustatory stimulus.

We present a case of facial pain associated with sweet stimulus. An immediate, electric-like, short, unilateral pain was evoked by strong sweet gustatory stimulation. This was followed 6 to 8 hours later by a bilateral severe headache associated with bilateral tearing, rhinorrhea, periorbital swelling, flushing, and photophobia that lasted up to 2 days. The immediate pain that was experimentally induced with 2.5 grams of sucrose placed on the tongue could be abolished with carbamazepine. However, carbamazepine did not prevent the headache complex that appeared 6 to 8 hours later. Conversely, a trial with indomethacin abolished the late-onset headache, but not the immediate neuralgic-type pain. The independent nature of these pains suggests different pathophysiological mechanisms which are discussed.

Preoperative prophylaxis for C1 esterase-inhibitor deficiency in patients undergoing oral surgery: a report of three cases.

C1-inhibitor deficiency, or hereditary angioedema, is a genetic disorder characterized by recurrent circumscribed, nonpruritic, nonpitting subepithelial edema. Minor trauma to the tissue, such as tooth extraction, can trigger life-threatening laryngeal edema. The use of fresh frozen plasma and/or danazol before treatment prevents angioedema attacks. A critical review of the treatment regimen and prophylaxis for C1-inhibitor deficiency is presented, and three new cases are described.

Idiopathic trigeminal pain associated with gustatory stimuli.

We present a unique case of a patient with facial pain evoked by gustatory stimuli. Pain was typically evoked by application of sucrose to the ipsilateral anterior 2/3 of the tongue, but not to the contralateral aspect. Pain was referred to the maxillary tuberosity area and, when stronger, to the infraorbital and supraorbital regions. Sucrose was most effective in eliciting pain, whilst saline, citric acid and water had a minimal effect. Spatial or temporal summation of gustatory stimuli was associated with stronger pain of longer duration and shorter latency. Some of the pain characteristics were similar to those of idiopathic trigeminal neuralgia. Thus, pain was elicited by innocuous ipsilateral stimuli, referred out of the stimulus zone, persisted beyond the period of stimulation and could be controlled with carbamazepine. We proposed a central neural mechanism for pain induction with convergence between gustatory stimuli afferents and pain pathways in the trigeminal system.

Dysgeusia, gustatory sweating, and crocodile tears syndrome induced by a cerebellopontine angle meningioma.

Facial nerve involvement in cerebellopontine angle tumors, both during their development and after excision, may be expressed in irreversible dysfunction of the parasympathetic pathways. The exact location of the lesion along the efferent nerve fibers can be established through evaluation of the functional level of those organs supplied by the cholinergic motor secretory components. This report deals with a female patient in whom peripheral facial palsy developed shortly after removal of a right cerebellopontine angle meningioma. She had slight facial asymmetry and deafness in the right ear and complained of prandial flush and sweating of the right malar area. Occult ipsilateral hyposalivation and hypolacrimation were diagnosed. In patients with seventh and ninth cranial nerve pathoses, evaluation of the end organs that are supplied by their associated autonomous nerve fibers is mandatory to prevent late ocular and oral sequelae.