Hepatic Lymphoma Preceded by Recurrent Multiple Cranial Neuropathy

No abstract available.

Diverse clinical manifestations caused by varicella-zoster virus reactivation / 영남의대학술지

The two distinctive clinical features of varicella-zoster virus (VZV) are varicella (chickenpox) by primary infection and zoster (singles) by the reactivation of latent infection. In addition to the two typical clinical symptoms mentioned above, diverse clinical manifestations have been reported as a result of VZV reactivation, including chronic radicular pain without rash, visual loss, facial palsy, dysphagia, sore throat, odynophagia, otalgia, hearing loss, dizziness, headache, hemiplegia, etc. Most of these symptoms are derived from neuropathy and vasculopathy of affected nerves and arteries. Diagnosis of VZV disease can be difficult if there is no appearance of a skin rash during development of atypical symptoms. In addition to natural infection, vaccination and anti-viral agent treatment have influenced the changes of epidemics and clinical presentations of varicella and zoster. In this article, diverse clinical manifestations caused by VZV reactivation, particular without skin rash, are reviewed.

Neurosyphilis Presenting with Multiple Cranial Neuropathy

Neurosyphilis can present with various clinical symptoms. We report a patient with multiple cranial neuropathy that, mimicked tuberculosis, but was finally diagnosed as neurosyphilis. A 38-year-old man was admitted due to subacutely progressive hearing loss. Brain MRI revealed multiple dural enhanced masses on contrast-enhanced T1 weighted images. Brain biopsy of the dural enhanced lesion revealed chronic granulomatous inflammation with coagulation necrosis, compatible with syphilitic gumma. Serum venereal disease research laboratory and fluorescent treponemal antibody absorption test results were positive. Treatment with penicillin resolved the patient's symptom.

A Case of Central Skull Base Osteomyelitis Concurrent with Multiple Lower Cranial Nerve Palsies / 대한이비인후과학회지

In most cases, skull base osteomyelitis arises from infections of external auditory canal, middle ear or paranasal sinuses. On the other hand, atypical or central skull base osteomyelitis has no evidence of external otitis or other infection sources. It is often found located on clivus and involves lower cranial nerves and brainstem through the foramina of skull base. The overall rate of mortality reaches 10% and long-term neurologic sequelae are seen in additional 31% of cases regardless of aggressive treatment. We recently encountered a 68-year-old man with right facial pain and generalized headache, and we achieved good outcome with the recovery of vocal cord palsy and disappearance of headache by surgical debridement and long-term antibiotics. We report it with a review of literature.

Case of Multiple Cranial Diabetic Neuropathies Involving the Third, Fourth and Sixth Cranial Nerves / 대한내과학회지

Multiple simultaneous cranial neuropathies occur rarely in diabetes patients. In general, diabetic cranial neuropathy presents in an isolated form and frequently involves oculomotor or facial nerves. We report a 73-year-old man with known type 2 diabetes mellitus who presented with severe dizziness, diplopia and third, fourth and sixth nerve ophthalmoplegia of both eyes. Radiological, laboratory and ophthalmic work-up including magnetic resonance imaging and angiography (MRI and MRA) revealed no specific tumor, aneurysm, or inflammation findings, except for a previous cerebral infarction and atherosclerotic changes in the internal carotid and vertebral arteries. After strict blood glucose control, the multiple cranial nerve palsies spontaneously resolved in 12 weeks. We report the case with a review of the literature.

Neurosarcoidosis after Uveitis

No abstract available.

Multiple Cranial Neuropathy with and Polyradiculoneuropathy as a Delayed Sequelae after of Ethylene Glycol Intoxication / 대한임상신경생리학회지

Multiple cranial and peripheral neuropathies as a delayed sequellae of ethylene glycol poisoning is a less well known clinical entity and its information about long-term electrophysiological and clinical outcomes is limited. We report a 45-year-old male who presented with acute renal failure and subsequently developed multiple cranial neuropathy, respiratory failure, and flaccid tetraparesis. Through sequential electrophysiological studies, we would like suggest that the main pathophysiology of ethylene glycol-related neuropathy is a demyelinating polyradiculoneuropathy with secondary axonal degeneration.

Clinical Outcome of Cranial Neuropathy in Patients with Pituitary Apoplexy

OBJECTIVE: Pituitary apoplexy (PA) is described as a clinical syndrome characterized by sudden headache, vomiting, visual impairment, and meningismus caused by rapid enlargement of a pituitary adenoma. We retrospectively analyzed the clinical presentation and surgical outcome in PA presenting with cranial neuropathy. METHODS: Twelve cases (3.3%) of PA were retrospectively reviewed among 359 patients diagnosed with pituitary adenoma. The study included 6 males and 6 females. Mean age of patients was 49.0 years, with a range of 16 to 74 years. Follow-up duration ranged from 3 to 20 months, with an average of 12 months. All patients were submitted to surgery, using the transsphenoidal approach (TSA). RESULTS: Symptoms included abrupt headache (11/12), decreased visual acuity (12/12), visual field defect (11/12), and cranial nerve palsy of the third (5/12) and sixth (2/12). Mean height of the mass was 29.0 mm (range 15-46). Duration between the ictus and operation ranged from 1 to 15 days (mean 7.0). The symptom duration before operation and the recovery period of cranial neuropathy correlated significantly (p = 0.0286). TSA resulted in improvement of decreased visual acuity in 91.6%, visual field defect in 54.5%, and cranial neuropathy in 100% at 3 months after surgery. CONCLUSION: PA is a rare event, complicating 3.3% in our series. Even in blindness following pituitary apoplexy cases, improvement of cranial neuropathy is possible if adequate management is initiated in time. Surgical decompression must be considered as soon as possible in cases with severe visual impairment or cranial neuropathy.

Arachnoid Cyst of the Velum Interpositum: Coincidence with Multiple Cranial Neuropathies: Case Report

Arachnoid cyst of the velum interpositum is unusual and causes symptoms similar to those seen with a third ventricular mass. This report describes a case in which the arachnoid cyst occupied the cistern of the velum interpositum and was coincident with multiple cranial neuropathies. The patient was treated by endoscopic fenestration of the cyst. The surgery resulted in decreased in the size of the cyst but aggravation of cranial neuropathies. The patient underwent methylprednisolone pulse therapy and intravenous immunoglobulin administration under the impression of the multiple cranial neuropathies and recovered completely 3 months later. The authors conclude that combined neurological disease that needs medical treatment should be differentiated and priority of the treatment should be determined carefully if arachnoid cyst is associated with unrelated or ambiguous neurological symptoms and signs. Careful considerations of cause and effect may avoid an unnecessary surgical manipulation

A case of neurosarcoidosis without systemic involvement

Sarcoidosis is a multisystem disorder of unknown cause. The involvement of the nervous system occurs 5% to 27% of patients with sarcoidosis, and neurosarcoidosis without systemic involvement is rare and difficult to diagnose. We present a case of 58-year-old woman with clinical features of multiple cranial and peripheral polyneuropathy with noncaseating granulomatous inflammation. Extensive testing for occult systemic sarcoidosis was negative. Sural nerve biopsy showed several perineural noncaseous granulomatous inflammation with prominent epithelioid cells. Oral steroid therapy led to some improvement. We report a patient with multiple cranial and peripheral polyneuropathy without systemic involvement, suspected sarcoidosis.

Combined Facial and Abducens Nerve Palsy in Pontine Infarction

Isolated cranial neuropathies involving the facial nerve are very rare manifestations of pontine infarction, and have not been described in paramedian pontine infarction. We report a 67-year-old woman who developed sudden and long-lasting right facial nerve paralysis accompanied by transient ipsilateral abducens nerve palsy. Brain magnetic resonance imaging showed two discrete simultaneous infarctions in the right inferior paramedian pontine area, which seemed to correspond to the facial nerve fascicle and the abducens nerve fascicle, respectively. Paramedian pontine infarction can be one of the causes of facial nerve palsy and present as an isolated or predominant sign.