Trigeminal Involvement Research Articles

Central trigeminal involvement in multiple sclerosis using high-resolution MRI at 3 T

Trigeminal neuralgia and sensory disturbance is common in multiple sclerosis (MS). Recent literature suggests that signal abnormalities in the cisternal trigeminal nerve and pontine root entry zone are seen in approximately 3% of MS patients, using conventional diagnostic MRI. The objective of this study was to determine the prevalence of trigeminal lesions using high-resolution MRI at 3T. Forty-seven patients with clinically definite MS, chosen at random from the outpatient population of a neuroscience centre underwent MRI on a Siemens 3T Trio machine. Three 3D sequences of T2 TSE (turbo spin echo), T2 FLAIR (fluid attenuated inversion recovery) and T1 IR (inversion recovery) were acquired in the coronal plane. The sequences were of contiguous 1 mm slices with in-plane resolution of up to 0.5 mm by 0.5 mm. Images were read by both a neurologist and a neuroradiologist. Any clinical history of trigeminal symptoms was determined for all subjects. The results showed that 11 patients (23%) had high signal in the trigeminal root entry zone and either the trans-cisternal nerve or pontine nucleus; example images are given. MRI changes did not correspond to clinical symptoms (chi square probability 1.000). The study concludes that high-resolution MRI at 3T yielded a high prevalence of detectable trigeminal abnormality in the MS sample studied. MRI involvement did not correspond to trigeminal symptoms.

Trigeminal neuralgia in an HIV patient

Trigeminal neuralgia is a painful condition affecting face. Its commonest cause is the tortuous vessels in prepontine cistern. There are other causes also, like brainstem lesions and mass lesions, as well as inflammatory causes. We present a case of an HIV patient with marked involvement of trigeminal nerves, which is a unique finding in immunocompromised patients.

Varicella Zoster Virus (VZV) in Solid Organ Transplant Recipients

-herpesvirus family. VZV is presentworldwide and is highly infectious. Primary infection leadsto acute varicella or ‘chickenpox,’ usually from exposureeither through direct contact with a skin lesion or throughairborne spread from respiratory droplets (1,2). After initialinfection, VZV establishes lifelong latency in cranial nerveanddorsalrootganglia,andcanreactivateyearstodecadeslater as herpes zoster (HZ) or ‘shingles’ (3). More than90% of adults in the United States acquired the disease inchildhood, while the majority of children and young adultshave been vaccinated with the live virus vaccine (2,4).Primary varicella typically presents with fever, constitu-tional symptoms and a vesicular, pruritic, widely dissem-inated rash that primarily involves the trunk and face (5).Thesymptomsusuallyresolvewithin7–10days,butinrarecases primary varicella leads to more severe disease andvisceral invasion. Complications, such as hepatitis, pancre-atitis, pneumonitis and encephalitis are infrequent but canbelife-threatening;adultsandveryyoungchildrenaremorelikely to develop such complications from primary infection(6,7). Rates of hospitalization and mortality due to varicellahave dropped with the institution of routine childhood vari-cella vaccination (8,9).Nearly all patients with HZ develop an exanthem of vesic-ular lesions in a dermatomal distribution. The annual inci-dence of HZ in the general population is 1.5–3.0 cases per1000 persons (2), and is estimated to occur in up to 20%of individuals during their lifetime (10). Secondary compli-cations such as bacterial superinfection and postherpeticneuralgia (PHN), or chronic neuropathic pain at the site ofHZ, lead to increased morbidity (11).Over 90% of adult solid organ transplant (SOT) recipientswill be seropositive for VZV. Rates are lower in pediatrictransplants(12,13),butimmunitywillincreaseasuptakeofvaricella vaccine improves. Varicella is rare in adult SOT re-cipients,butcanbedevastating,withvisceralinvolvement,severe skin disease, and disseminated intravascular coag-ulation (14–19). HZ is a frequent infectious complication inSOT recipients with an incidence of approximately 8–11%during the first 4 years posttransplant (20–22). Invasive dis-ease and dissemination similar to that seen in primary VZVinfection are uncommon but have been reported in SOTand other immunocompromised populations, and level ofimmunosuppression may alter the risk of developing thesecomplications (17,23,24). Rates of PHN in SOT recipi-ents may also be higher than in immunocompetent popu-lations (22).

Trigeminal nerve palsy in nasopharyngeal carcinoma: Correlation between clinical findings and magnetic resonance imaging

Our aim was to document the relationship between clinical and MRI evidence of trigeminal nerve involvement. The MRI and medical records of 924 consecutive patients with newly diagnosed nasopharyngeal carcinoma (NPC) were reviewed retrospectively. A total of 92 divisions of palsied trigeminal nerves were found clinically in 46 patients (5.0%). The involved trigeminal nerve was ophthalmic nerve (V1; n = 21), the maxillary division (V2; n = 41), and the mandibular division (V3; n = 30). Of the 316 patients with MRI-demonstrated trigeminal nerve involvements, the symptoms were lacking in 270 patients (85.4%). Of the 92 clinical palsied trigeminal nerve divisions, 91 nerves (98.9%) showed MRI evidence of 1 or more trigeminal nerve involvements. Of the 91 palsied trigeminal nerve with MRI evidence, 85 divisions (93.4%) were found with intracranial or orbital segment involvement, 6 (6.6%) divisions were found only basicranial evidence, and 83 (91.2%) divisions were found with cavernous sinus invasion. The incidence of MRI-evidenced trigeminal nerve involvement is high and often asymptomatic in NPC. Almost all patients with clinical trigeminal nerve palsies had MRI evidence of trigeminal nerve involvement in intracranial or orbital segment, especially in cavernous sinus.

The Use of Implants in Facial Augmentation for Hemifacial Atrophy

The Use of Implants in Facial Augmentation for Hemifacial Atrophy

Retinal metastases treated with lapatinib (L) in a young HER2-positive breast cancer patient: Case report

12008 Background: The incidence of ocular metastases (OM) in patients with metastatic breast cancer (BC) is reported to be as high as 30% and is usually associated with short-term fatal outcome and severe impairment of quality of life. OM, predominantly involving the choroids, can be the first sign of systemic spread but are rarely reported, suggesting absent/mild clinical signs and difficult diagnosis. Despite the advances in surgery and radiation therapy, novel therapeutic strategies are eagerly needed to improve the treatment of central nervous system (CNS) metastases, especially of OM, and to reduce side effects. Women with HER2-positive BC are known to have a high incidence of CNS relapse despite effective systemic control with Trastuzumab (T). L is an oral dual tyrosine kinase inhibitor which selectively inhibits both HER1 and HER2 growth factor receptors. The L small molecular size (580 kDa) allows its penetrating the blood-brain barrier and L has been proven to be effective against CNS metastases with an acceptable safety profile and in particular no neurological toxicity. Methods: A 37-year-old woman, shortly after completion of T plus Paclitaxel-Paraplatin chemotherapy for HER2-positive metastatic BC (lung, liver, and bone), complained of rapid decrease of visual acuity with subsequent blindness and local pain which proved to be related to bilateral retinal metastases, without additional intracranial involvement or systemic progression. The patient started L plus capecitabine (X) at recommended doses with significant gastrointestinal toxicity (diarrhoea, gastric pain, dehydration): the dose of X was then reduced to 1,500 mg total daily dose with sustained L at 1,250 mg/daily. Results: visual acuity quickly recovered after treatment start and a complete retinal response was documented after 3 months’ therapy with stable systemic disease. After 6 months’ therapy the patient developed basal skull and trigeminal involvement with no retinal and CNS recurrence or systemic progression. Conclusions: L demonstrated to be a rapidly effective treatment option for this underreported intracranial sanctuary, with a good safety profile as compared to standard current therapies. No significant financial relationships to disclose.

Aspects TDM et IRM du kyste arachnoïdien de l’apex pétreux: À propos de trois cas

Purpose To describe the CT and MRI features of 3 cases of arachnoid cyst of the petrous apex. Patients and methods Three patients with isolated trigeminal neuralgia, trigeminal hypoesthesia, and sinusitis. Axial and coronal CT images were obtained. T1W, FSE T2W, FLAIR, T2*W and diffusion-weighted MR sequences were obtained. Results In all cases, both CT and MRI showed expansile lesions eroding the petrous apex. Lesions were hypodense on CT and isointense to CSF on MRI, without contrast enhancement. In one case, the lesion was contiguous with Meckel's cave with temporal fossa and sphenoid sinus extension. CT and MR imaging features are useful to distinguish arachnoid cysts of the petrous apex from other benign lesions of the petrous apex. Conclusion CT and MRI imaging features allow diagnosis of arachnoid cyst of the petrous apex because its imaging features, especially on DWI, are different from other cystic lesions of the petrous apex, namely cholesteatoma. It should be considered in patients with trigeminal involvement, especially trigeminal neuralgia.

Pontine tegmental cap dysplasia: a novel brain malformation with a defect in axonal guidance

Four unrelated children are described with an identical brainstem and cerebellar malformation on MRI. The key findings are: vermal hypoplasia, subtotal absence of middle cerebellar peduncles, flattened ventral pons, vaulted pontine tegmentum, molar tooth aspect of the pontomesencephalic junction and absent inferior olivary prominence. Peripheral hearing impairment is present in all. Variable findings are: horizontal gaze palsy (1/4), impaired swallowing (2/4), facial palsy (3/4), bilateral sensory trigeminal nerve involvement (1/4), ataxia (2/4). Bony vertebral anomalies are found in 3/4. Additional MR studies in one patient using diffusion tensor imaging (DTI) with colour coding and fibre tracking revealed an ectopic transverse fibre bundle at the site of the pontine tegmentum and complete absence of transverse fibres in the ventral pons. The combined findings indicate an embryonic defect in axonal growth and guidance. Phenotypic analogy to mice with homozygous inactivation of Ntn1 encoding the secreted axonal guidance protein netrin1, or Dcc encoding its receptor Deleted in Colorectal Cancer led us to perform sequence analysis of NTN1 and DCC in all the patients. No pathogenic mutations were found. For the purpose of description the name 'pontine tegmental cap dysplasia' (PTCD) is proposed for the present malformation, referring to its most distinguishing feature on routine MRI.

Perioperative Pain Management in Patients Undergoing Skull Base Tumor Resection

Introduction: The perioperative pain associated with skull base tumors can produce significant morbidity affecting recovery and quality of life before and after surgery. Trigeminal nerve involvement with facial pain or difficulty swallowing may be observed with many neoplasms. In addition, headache with associated diplopia are also common presurgical problems. Postoperative pain, after skull base procedures, has been noted to occur in 65 to 85% of patients. This report examines treatment options for pain control prior to surgery and also evaluates postoperative treatment modalities for pain. Methods and Observations: The management of trigeminal pain may include the use of drugs such as carbamazepine, gabapentin, balofen, lamotrigine, and others. In addition, percutaneous techniques such as radio frequency ablation are used to reduce facial pain associated with tumor involvement of the nerve. The use of trigger point injections along with nerve block therapies will also be discussed. Dorsal root entry zone deafferentation procedures (DREZ) along with their effect on reducing intractable face pain will be described. Postoperative pain control is effectively accomplished with the use of patient-controlled analgesia (PCA) with or without the addition of antiemetics. PCA has been shown to reduce postoperative pain scores and the use of rescue analgesics for pain. Increased satisfaction scores with pain treatment after skull base surgery has been demonstrated with the use of PCA compared to bolus dose analgesic treatment (7.5 ± 2.2 vs. 5.5 ± 3.2, P = 0.006). The effect of other nonopioid therapies such as acetaminophen, nonsteroidal anti-inflammatory agents, cox-2 inhibitors, neurostimulants, and antidepressants will also be described for the treatment of pain after skull base resection. Nerve block therapy, the use of acupuncture, and other nonpharmacologic treatments, including biofeedback and relaxation techniques, will also be discussed. Conclusion: This report describes pain and its treatment in patients with skull base pathology in both the pre- and postoperative settings. Analgesic techniques are described and compared for efficacy and outcome. Best practice opportunities include the use of PCA narcotics for postoperative pain with carbamazepine and nerve block therapies used for preoperative pain control.

Neurophysiological evaluation of trigeminal and facial nerves in patients with chronic inflammatory demyelinating polyneuropathy

Cranial neuropathy is clinically uncommon in patients with chronic inflammatory demyelinating polyneuropathy (CIDP), but there is little information on the neurophysiological examination of cranial nerve involvement. To determine the incidence of trigeminal and facial nerve involvement in patients with CIDP, the direct response of the orbicularis oculi muscle to percutaneous electric stimulation of the facial nerve and the blink reflex (induced by stimulation of the supraorbital nerve) were examined in 20 CIDP patients. The latency of the direct response was increased in 12 patients (60%) and an abnormal blink reflex was observed in 17 patients (85%). There was no correlation between electrophysiological findings and the latencies of the direct and R1 responses and disease duration or clinical grade in CIDP patients. Nevertheless, the prevalence of subclinical trigeminal and facial neuropathy is extremely high in patients with CIDP when examined by neurophysiological tests.

Trigeminal Somatosensory Evoked Potentials in Multiple Sclerosis: A Case Report

Somatosensory evoked potentials elicited by trigeminal nerve stimulation (TSEPs) allow the study of the trigeminal system, its peripheral to its central portion. As a routine clinical testing procedure, however, this method has not yet received greater attention and still has to wait to become a part of the diagnostic workup in multiple sclerosis (MS). A patient diagnosed as MS was presented with selective involvement of the left trigeminal nerve. Neurophysiologically, the most prominent and persistent abnormalities were found in the TSEPs. The presumed diagnosis of MS was subsequently confirmed by MRI showing evidence of demyelinating disease. There has been a scarcity of references on TSEP. Our study emphasizes its usefulness and a plea is being made for the inclusion of TSEP in protocols for the diagnostic workup in patients with MS.

Painful Neuropathy with Trigeminal Nerve Involvement in Type 2 Diabetes

After several years of treatment for type 2 diabetes mellitus, a 69-year-old Japanese man developed an acute painful neuropathy, characterized by bilateral causalgia and dysaesthesia in his cheeks and around his eyes, typically 30 min to 3 h after meals. As his glycaemic control deteriorated, his haemoglobin (Hb) A1c level gradually increased from 7 - 8% to 10.3% and his symptoms became more severe. The pain radiated out along the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve. The patient was treated with insulin therapy and his HbA1c level decreased from 10.3% to 6.8% within 7 months. Five months after initiating insulin therapy, his symptoms showed a dramatic improvement. This was a very unusual case of bilateral acute painful neuropathy that involved the ophthalmic and maxillary divisions of the trigeminal nerve, and in which aggravation of the symptoms clearly related to poor glycaemic control.

Numb cheek syndrome as the first manifestation of anti–Hu paraneoplastic neuronopathy

Sirs: Unilateral numb cheek syndrome (NCS) has rarely been described as the first manifestation of malignancy due to neoplastic involvement of the trigeminal nerve, more specifically the maxillary branch [1, 2]. NCS as the first symptom of subacute paraneoplastic sensory neuronopathy has, to the best of our knowledge, never been reported. We present this case because its rarity led to a diagnostic delay of several months. A 47-year-old man presented with a one month history of numbness in the left cheek, both inner and outer surfaces. The area of numbness corresponded with the mandibular division of the left trigeminal nerve (V3). His medical history was unremarkable. Neurological examination was normal including the left V3 area. As the main part of the cheek is innervated by the buccal nerve we considered that our patient had a mandibular sensory neuropathy probably due to compression or infiltration of the nerve by local malignancy, as seen in other types of trigeminal mononeuropathy [3]. Ancillary investigations including contrast enhanced brain MRI, thorax CT and extensive laboratory examinations of the blood and urine were normal. Cerebrospinal fluid (CSF) examination revealed mild lymphocytic pleocytosis, slightly elevated protein of 0.69 g/l (0.2–0.5) and no malignant cells or oligoclonal bands. Although intracranial malignancy could not be ruled out an expectant policy was chosen by the patient. Two months later he complained of slightly unsteady gait. A second MRI of the brain and skull base was normal. Another 4 months later he noticed numbness of his left hand and foot. Neurological examination showed only left sided facial hypalgesia. Nerve conduction studies were consistent with a non uniformly distributed, predominantly axonal, sensorimotor neuropathy, most pronounced in the left extremities. Repeated conventional CSF examination only showed an increased protein level of 0.86 g/l. Anti-Hu antibodies in CSF were detected with indirect immunofluorescence and Western blotting techniques. A second thorax CT and whole body PET-scan eventually showed a solitary lesion in the right hilus, which proved to be a metastasis of an anaplastic small cell carcinoma on histological examination. Although the primary tumour remained unrevealed, a paraneoplastic multifocal mainly sensory neuronopathy associated with presumed primary small cell lung carcinoma was diagnosed and combined chemotherapy started. Fifteen months after the initial complaint the primary tumour remained undetected and no metastases were found. The neuropathy progressed resulting in very severe sensorimotor neuropathy with asymmetric painful paresthesias, diffuse proprioceptive loss and weakness in all extremities. In patients with paraneoplastic anti-Hu associated neuropathy (AHN) involvement of the cranial nerves may be present but is very rarely the presenting symptom. AHN most commonly presents as a subacute sensory neuropathy, less frequently as a sensorimotor neuropathy [5, 6]. These neurological symptoms typically antedate the diagnosis of cancer and most commonly involve the extremities [4–7]. In 306 patients with malignancy and associated anti-Hu antibodies, 50 % of the patients had a sensory neuropathy [4–6]. Three of them had trigeminal nerve involvement, but in no one was cheek numbness described as the only presenting symptom. As initially no primary tumour was found, we did not consider AHN as a potential cause of the unilateral cheek numbness in our patient. The final diagnosis was reached because of the extension of the sensory symptoms and eventually the evidence of an asymmetric sensorimotor neuropathy. The diagnostic delay between the NCS and final diagnosis was 6 months, which lies within the range of reported diagnostic delays in AHN patients [4–7]. As early treatment of the underlying malignancy is the mainstay of treatment, we report this patient in order to add NCS to the list of presenting symptoms of AHN.

Trigeminal involvement in multiple sclerosis: magnetic resonance imaging findings with clinical correlation in a series of patients

Trigeminal involvement detected by magnetic resonance imaging (MRI) in multiple sclerosis (MS) patients is usually associated with trigeminal neuralgia (TN) or painless paraesthesia in the trigeminal distribution. Our aim is to review the incidence of trigeminal involvement on MRI in a series of patients with MS at our institution, with further clinical correlation. We reviewed MRI scans of 275 MS patients for the presence of gadolinium enhancement on postcontrast T1-weighted images, anatomical and signal abnormalities on different sequences at the pontine trigeminal root entry zone (REZ) and in the cisternal portion of the nerves. We observed enhancement in the cisternal portion of the nerves and signal abnormalities (with or without enhancement) at the pontine trigeminal REZ in 8 (2.9%) patients, and enhancement was bilateral in 6 (75%) of those. Despite the inflammatory activity, none of them had TN and 3 (37.5%) had only painless paraesthesias in the correspondent V3 distribution. We also found a marked trigeminal hypertrophy in 2 (25%) patients, both with a longer period of disease. Our results confirm a high and clinically silent incidence of trigeminal involvement in MS patients, and suggest a simultaneous role of the central and peripheral type of myelin in trigeminal demyelination.

Alveolar Bone Necrosis and Tooth Exfoliation Following Herpes Zoster Infection: A Review of the Literature and Case Report

Herpes zoster (HZ) presents as a cutaneous vesicular eruption in the area innervated by the affected sensory nerve, usually associated with severe pain. Oral manifestations of HZ appear when the mandibular or maxillary divisions of the trigeminal nerve are affected. This is a case report of a 63-year-old woman with HZ infection with trigeminal nerve involvement that led to a rapid loss of alveolar bone and exfoliation of two teeth. The initial intraoral examination showed redness of the alveolar mucosa and gingiva of the lower right quadrant with multiple well-delimited and painful erosive lesions affecting the attached gingiva around the teeth. Two weeks later, teeth number 27 (lower right canine) and 28 (lower right first premolar) had class III mobility, flow of purulent exudate from the gingival sulcus, and deep pockets (>11 mm). The radiological examination showed advanced alveolar bone loss around both teeth. The prognosis for teeth number 27 and 28 was considered hopeless, and they were extracted. Due to extensive necrosis there was no interdental alveolar bone. The case is presented with a review of clinical data from patients with trigeminal HZ infection associated with osteonecrosis or exfoliation of teeth previously reported in the literature. The mechanisms by which the HZ infection leads to the alveolar bone necrosis are discussed. Extensive osteonecrosis and exfoliation of teeth in the area innervated by the nerve affected by HZ has been reported after HZ infection. Clinicians should be aware of this possible outcome after a trigeminal HZ infection.

CSF flow study in Chiari I malformation.

The aim of this prospective study was to define the role of cardiac gated phase-contrast ciné magnetic resonance imaging in deciding the therapeutic strategy in patients with Chiari I malformation. Twenty-one patients operated on between February 2000 and July 2002 were enrolled in the study. All patients underwent a detailed preoperative neurological examination. MRI of the craniovertebral junction and the whole spine was done, followed by cardiac gated phase contrast ciné magnetic resonance imaging. Signs and symptoms of syringomyelia were noted in 15 patients and cerebellar signs in 11 patients. Three of them had trigeminal nerve involvement, and 4 had ninth and tenth cranial nerve involvement. The sixth and accessory nerves were involved in 1 patient each. Preoperative CSF flow studies revealed obstructive flow both anteriorly and posteriorly in 6 patients and only posterior block in 15 patients. One patient investigated for failed foramen magnum decompression revealed obstruction to CSF flow ventrally. Foramen magnum decompression with duroplasty was done in all these cases. The patient who had a persistent ventral flow block underwent odontoidectomy. Patients were followed up for a maximum of 36 months, with a mean of 18 months. MRI CSF flow studies revealed established flow dorsally in all cases. Seventeen patients showed clinical improvement and 2 of them did not show any neurological changes. Two patients deteriorated following an initial period with a shunt. MRI CSF flow study is an effective tool for deciding the type of surgery to be performed and also for monitoring patients postoperatively.

Trigeminal nerve involvement in T-cell acute lymphoblastic leukemia: value of MR imaging

A 30-year-old male with T-cell acute lymphoblastic leukemia presented with facial numbness. Neurological examination revealed paresthesia of the left trigeminal nerve. Cerebrospinal fluid (CSF) cytology showed no atypical cells. Gadolinium-enhanced magnetic resonance (MR) imaging demonstrated enlargement and enhancement of intracranial portions of the left trigeminal nerve. The abnormal MR imaging findings almost completely resolved after the chemotherapy. Gadolinium-enhanced MR imaging is not only a useful procedure for the early diagnosis of cranial nerve invasion by leukemia but it might be helpful to follow the changes after the treatment.

Giant Cavernous Carotid Aneurysms

To review the presenting symptoms and ophthalmic findings of 57 patients with cavernous carotid aneurysms of giant size (> or = 2.5-cm diameter). Hospital charts of 57 patients with giant cavernous carotid aneurysms who presented to University Hospital in London, Ontario, Canada between 1961 and 1993 were reviewed. All patients were proven by cerebral angiography to have unruptured giant cavernous carotid aneurysms. Forty-six patients (81%) were women (mean age, 54 years). The most common presenting symptoms were diplopia (89%), retroorbital pain (61%), headache (19%), diminished or blurred vision (14%), and photophobia (4%). The most common clinical sign was partial or complete ophthalmoplegia (93%). Trigeminal nerve involvement was found in 37% of patients. Other clinical signs included ptosis, decreased visual acuity, proptosis, and visual field defects. This study characterizes a large group of patients with giant cavernous carotid aneurysms seen over a 30-year period at a single institution. As in previous studies, diplopia and retroorbital pain were the most common symptoms. The high incidence of ophthalmoplegia observed in this study may be explained by a greater compressive and/or ischemic effect of giant aneurysms compared with their smaller counterparts.

Giant Cavernous Carotid Aneurysms

Objectives: To review the presenting symptoms and ophthalmic findings of 57 patients with cavernous carotid aneurysms of giant size (≥2.5-cm diameter). Materials and Methods: Hospital charts of 57 patients with giant cavernous carotid aneurysms who presented to University Hospital in London, Ontario, Canada between 1961 and 1993 were reviewed. All patients were proven by cerebral angiography to have unruptured giant cavernous carotid aneurysms. Results: Forty-six patients (81%) were women (mean age, 54 years). The most common presenting symptoms were diplopia (89%), retroorbital pain (61%), headache (19%), diminished or blurred vision (14%), and photophobia (4%). The most common clinical sign was partial or complete ophthalmoplegia (93%). Trigeminal nerve involvement was found in 37% of patients. Other clinical signs included ptosis, decreased visual acuity, proptosis, and visual field defects. Conclusions: This study characterizes a large group of patients with giant cavernous carotid aneurysms seen over a 30-year period at a single institution. As in previous studies, diplopia and retroorbital pain were the most common symptoms. The high incidence of ophthalmoplegia observed in this study may be explained by a greater compressive and/or ischemic effect of giant aneurysms compared with their smaller counterparts.

Cancer pain: a neurological perspective.

Nerve pain in cancer is common, mainly manifested by a radiculopathy associated with vertebral metastasis, by a plexopathy caused by lymph-node involvement or, more rarely, by trigeminal involvement in cancer of the head and neck. Less frequent types of nerve pain can occur as late effects of antitumour therapy, including surgery, radiation and chemotherapy. The distinction between a nociceptive and a non-nociceptive nerve pain helps in determining the most appropriate symptomatic management.