Wegener granulomatosis involving the pterygopalatine fossa: an unusual case of trigeminal neuropathy.
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We report on a case of Wegener granulomatosis in the pterygopalatine fossa that was associated with trigeminal neuropathy. MR and CT examinations were useful in depicting the extent of the lesion and suggesting a perineural spread. Diagnosis was confirmed with positive serum assay findings for the presence of cytoplasmic antineutrophil cytoplasm antibody. (+info)
A case of multiple schwannomas of the trigeminal nerves, acoustic nerves, lower cranial nerves, brachial plexuses and spinal canal: schwannomatosis or neurofibromatosis?
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In most cases, while schwannoma is sporadically manifested as a single benign neoplasm, the presence of multiple schwannomas in one patient is usually indicative of neurofibromatosis 2. However, several recent reports have suggested that schwannomatosis itself may also be a distinct clinical entity. This study examines an extremely rare case of probable schwannomatosis associated with intracranial, intraspinal and peripheral involvements. A 63-year-old woman presented with a seven-year history of palpable lumps on both sides of the supraclavicular area and hearing impairment in both ears. On physical examination, no skin manifestations were evident. Facial sensory change, deafness in the left ear and decreased gag reflex were revealed by neurological examination. Magnetic resonance imaging revealed multiple lesions of the trigeminal nerves, acoustic nerves, lower cranial nerves, spinal accessory nerve, brachial plexuses, and spinal nerves. Pathological examination of tumors from the bilateral brachial plexuses, the spinal nerve in the T8 spinal position and the neck mass revealed benign schwannomas. Following is this patient case report of multiple schwannomas presenting with no skin manifestations of neurofibromatosis. (+info)
Raeder's syndrome [corrected]: paratrigeminal paralysis of the oculopupillary sympathetic system.
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Raeder described five patients with mixed features of trigeminal nerve pathology and oculosympathetic impairment, with or without other cranial nerve lesions. This constellation of clinical features drew the original author's attention to the paratrigeminal region as a likely site for the causative lesion in this syndrome. An analysis of the anatomy of the oculosympathetic innervation supports the view that a restricted lesion in the middle cranial fossa might cause the syndrome of trigeminal nerve involvement, neuralgic pain or sensory change, with ptosis or miosis, or both, but no anhidrosis. Such a paratrigeminal oculosympathetic syndrome (POSS) usefully reminds clinicians to pursue vigorously possible lesions of the middle cranial fossa with careful, and possibly repeated, imaging studies. Attaching the eponym Raeder's syndrome or Raeder's paratrigeminal neuralgia to this syndrome adds nothing valuable to the anatomical description (POSS), which might be preferred for clarity. (+info)
Hemimasticatory spasm treated with botulinum toxin: case report.
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We describe a female patient with hemimasticatory spasm, a rare movement disorder due to dysfunction of the motor trigeminal nerve of unknown origin. This patient had an excellent response to botulinum toxin therapy. (+info)
Trigeminal and polyradiculoneuritis in a dog presenting with masticatory muscle atrophy and Horner's syndrome.
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A 9-year-old, spayed female, Airedale Terrier was euthanatized and necropsied after a progressive clinical course that included Horner's syndrome of the left eye and unilateral atrophy of the masticatory muscles. Although gross lesions were limited, a polyradiculoneuritis and ganglionitis that was most severe in the trigeminal nerves and ganglia were confirmed histologically. The inflammatory infiltrate consisted predominantly of macrophages and B and T lymphocytes that were phenotypically confirmed by immunostaining. Horner's syndrome was the result of damage to postganglionic sympathetic fibers that were incorporated in segments of the inflamed trigeminal nerve and its ophthalmic branch. Histologically, the character and distribution of the inflammation was similar to previously described syndromes of suspected immune-mediated etiology in humans and animals. (+info)
Clinical manifestations and treatment considerations of herpes simplex virus infection.
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Herpes simplex viruses (HSV) types 1 and 2 cause infections manifesting as dermatologic, immunologic, and neurologic disorders. Some of the most important manifestations and complications of HSV infection are considered here in a neuroanatomic context. This discussion should aid in understanding the pathogenesis and, in some cases, diagnosis and management of associated HSV-related diseases. The sensory nervous system, rather than skin and mucous membranes, is the primary target of HSV infection. With the intention of extending the benefits of acyclovir, valacyclovir is now being explored in a number of HSV-related conditions. This review extends contemporary thinking about how new antiherpetic drugs might be put to greater therapeutic use in the future. (+info)
The antimigraine 5-HT 1B/1D receptor agonists, sumatriptan, zolmitriptan and dihydroergotamine, attenuate pain-related behaviour in a rat model of trigeminal neuropathic pain.
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1. Peripheral lesion to the trigeminal nerve may induce severe pain states. Several lines of evidence have suggested that the antimigraine effect of the triptans with 5-HT(1B/1D) receptor agonist properties may result from inhibition of nociceptive transmission in the spinal nucleus of the trigeminal nerve by these drugs. On this basis, we have assessed the potential antinociceptive effects of sumatriptan and zolmitriptan, compared to dihydroergotamine (DHE), in a rat model of trigeminal neuropathic pain. 2. Chronic constriction injury was produced by two loose ligatures of the infraorbital nerve on the right side. Responsiveness to von Frey filament stimulation of the vibrissal pad was used to evaluate allodynia. 3. Two weeks after ligatures, rats with a chronic constriction of the right infraorbital nerve displayed bilateral mechanical hyper-responsiveness to von Frey filament stimulation of the vibrissal pad with a mean threshold of 0.38+/-0.04 g on the injured side and of 0.43+/-0.04 g on the contralateral (left) side (versus > or =12.5 g on both sides in the same rats prior to nerve constriction injury). 4. Sumatriptan at a clinically relevant dose (100 microg kg(-1), s.c.) led to a significant reduction of the mechanical allodynia-like behaviour on both the injured and the contralateral sides (peak-effects 6.3+/-1.1 g and 4.4+/-0.7 g, respectively). A more pronounced effect was obtained with zolmitriptan (100 microg kg(-1), s.c.) (peak-effects: 7.4+/-0.9 g and 3.2+/-1.3 g) whereas DHE (50-100 microg kg(-1), i.v.) was less active (peak-effect approximately 1.5 g). 5. Subcutaneous pretreatment with the 5-HT(1B/1D) receptor antagonist, GR 127935 (3 mg kg(-1)), prevented the anti-allodynia-like effects of triptans and DHE. Pretreatment with the 5-HT(1A) receptor antagonist, WAY 100635 (2 mg kg(-1), s.c.), did not alter the effect of triptans but significantly enhanced that of DHE (peak effect 4.3+/-0.5 g). 6. In a rat model of peripheral neuropathic pain, which consisted of a unilateral loose constriction of the sciatic nerve, neither sumatriptan (50-300 microg kg(-1)) nor zolmitriptan (50-300 microg kg(-1)) modified the thresholds for paw withdrawal and vocalization in response to noxious mechanical stimulation. 7. These results support the rationale for exploring the clinical efficacy of brain penetrant 5-HT(1B/1D) receptor agonists as analgesics to reduce certain types of trigeminal neuropathic pain in humans. (+info)
Pathological laughter in a patient with trigeminal neurinoma.
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We present a 47-year-old woman with a long history of anxiety and a more recent history of shock-like facial pain and episodes of laughter without any motivation. She could not explain the laughing bursts and did not have a sense of mirth preceding it. On neurological examination she presented a VI nerve palsy and trigeminal hypoesthesia (V2 and V3) on the right side. Magnetic resonance imaging exhibited a large cystic lesion on the right middle fossa causing significant compression on the brain stem. A frontoorbitozygomatic and pretemporal combined approach was performed. During intra and extradural exploration a large tumor was found on the trigeminal nerve. The whole lesion was resected, revealing to be a neurinoma on pathological exhamination. She maintained a VI nerve palsy but had complete remission of the unmotivated laughing episodes during the one year follow up. (+info)