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1/13. Hyperactive rhizopathy of the vagus nerve and microvascular decompression. Case report.

    A 37-year-old woman underwent microvascular decompression of the superior vestibular nerve for disabling positional vertigo. Immediately following the operation, she noted severe and spontaneous gagging and dysphagia. Multiple magnetic resonance images were obtained but failed to demonstrate a brainstem lesion and attempts at medical management failed. Two years later she underwent exploration of the posterior fossa. At the second operation, the vertebral artery as well as the posterior inferior cerebellar artery were noted to be compressing the vagus nerve. The vessels were mobilized and held away from the nerve with Teflon felt. The patient's symptoms resolved immediately after the second operation and she has remained symptom free. The authors hypothesize that at least one artery was shifted at the time of her first operation, or immediately thereafter, which resulted in vascular compression of the vagus nerve. To the authors' knowledge, this is the first reported case of a hyperactive gagging response treated with microvascular decompression. The case also illustrates the occurrence of a possibly iatrogenic neurovascular compression syndrome.
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2/13. Trigeminal pain caused by a cerebellopontine-angle lipoma. Case report and review of the literature.

    A 16-year-old girl complained of 2-year history of right facial pain, episodic vertigo and progressive hearing loss in the right ear. The facial pain was described as an episodic lancinating event confined to the second and third branch of the right trigeminal nerve. Computed tomography and magnetic resonance imaging revealed a 2 cm lesion in the right cerebellopontine-angle. At surgery, a soft, yellowish mass was found incorporating the 7th and 8th cranial nerves. The anterior-inferior cerebellar artery (AICA) was displaced medially and pushed into the sensory portion of the trigeminal nerve root, causing vascular compression. The hearing loss remained unchanged. The trigeminal pain disappeared over a period of several weeks. patients can be harmed in an attempt to remove these neurovascular nonmalignant, generally non growing, fatty vascular lumps. Only a partial, meticulous removal should be performed with a maximum effort to decompress the affected nerve.
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3/13. Recurrent arachnoid cyst of Meckel's cave mimicking a brain stem ischaemia. Report of a rare case.

    A 44-years old man developed TIA-like symptoms with dysaesthesia around the mouth, vertigo and diplopia. MRI revealed a cystic space-occupying lesion on the right Meckel's cave, which spread out into cerebellopontine angle in a further examination. Therefore surgical exploration was performed using a suboccipital approach. An arachnoidal cyst was found and removed including its wall. About three months later the patient suffered again from dysaesthesias of the right side of the face and a new MRI revealed a recurrence of the lesion, with extension into the cerebellopontine angle, too. Surgical revision was done using the same approach and the recurrent cyst was removed. Postoperatively, there were a transient hypaesthesia in the distribution area of the right trigeminal nerve and a light pulmonary embolism occurred as a complication. No symptoms have returned during an observation period of 15 months. CONCLUSION: An arachnoidal cyst must be considered as a rare cause, when a lesion is found at the Meckel's cave with intermittent clinical symptoms of a trigeminal nerve affection. As surgical treatment we favour fenestration and cyst wall resection.
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4/13. Syringobulbia: a surgical appraisal.

    Syringobulbia is a term which has been clinically applied to brain stem symptoms or signs in patients with syringomyelia. Syringobulbia clefts are found on investigation or at necropsy caused by cutting outwards of the CSF under pressure from the fourth ventricle into the medulla. These should be differentiated from the ascending syringobulbia which may occur from upward impulsive fluid movements in a previously established syringomyelia. Clinical analysis of 54 patients suggests that bulbar features are most often found with neither of the above mechanisms but are due to the effects of pressure differences acting downward upon the hind-brain with consequent distortion of the cerebellum and brainstem, traction on cranial nerves or indentation of the brain-stem by vascular loops. The commonest symptoms in the 54 patients were headache (35), vertigo (27), dysphonia or dysarthria (21), trigeminal paraesthesiae (27), dysphagia (24), diplopia (16), tinnitus (11), palatal palsy (11) and hypoglossal involvement (11). Careful attention to hydrocephalus is advisable before craniovertebral surgery, but the decompression of the hindbrain and the correction of craniospinal pressure dissociation remains the mainstay of surgical treatment. The results of careful surgery are good, 45 of the 54 cases reported improvement. Most of the reported deterioration occurred in a few patients who did conspicuously badly.
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5/13. Unilateral compression neuropathy of the hypoglossal nerve due to head suspension orthosis in mitochondriopathy.

    An 85-year-old woman with multisystem mitochondriopathy experienced tension headache, cervical pain, torque head-posture, and vertigo since 1980 for which she was continuously wearing a head-suspension-orthosis- since 1990. Since 1996 she developed severe left-sided weakness and wasting of the tongue. Needle-EMG of the left genioglossus muscle revealed abnormal spontaneous activity and reduced interference-pattern. No morphological alterations in the anatomical course of the hypoglossal nerve were found. Severe, unilateral weakness and wasting of the tongue was interpreted due to chronic compression of the hypoglossal nerve by long-standing use of a head-suspension-orthosis for cervical pain from cervical muscle weakness and resulting spinal degeneration.
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6/13. Recurrent vertigo in extrinsic compression of the brain stem.

    We present four patients who suffered from recurrent vertigo crises, which in most cases lasted hours or even days. In all of them the coincident finding was the presence of vascular compression of the brainstem (mainly vertebral dolichoectasia). Given the fact that the vertigo was always episodic and in that in the two cases where a treatment with carbamazepine could be used the result was the total suppression of the crises, we propose an ictal mechanism for them. Our findings differ from previous descriptions because: 1) the crises last longer, hours or even days, and 2) the involvement of the brainstem structures was extrinsic.
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keywords = vertigo
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7/13. The retrolabyrinthine approach and vascular loop.

    Several researchers have made progress toward determining the cause of hemifacial spasm, tinnitus, and episodic vertigo. During the past 5 years, we have encountered a vascular loop in six of 36 patients who were undergoing retrolabyrinthine vestibular neurectomy for recurrent disequilibrium and vertigo. In five of these six patients, disequilibrium improved after neurectomy. This report describes the clinical symptomatology and the results of preoperative cochleovestibular testing for those patients found intraoperatively to have a vascular loop and suspected neurovascular compression syndrome. Audiograms, although varied, characteristically did not demonstrate the low-frequency sensorineural hearing loss characteristic of Meniere's disease. No preoperative marker, with the single exception of computed tomography pneumocisternography, dependably predicted the presence of a vascular loop.
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keywords = vertigo
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8/13. vertigo caused by basilar artery compression of the eighth nerve.

    Vascular compression syndromes in the posterior cranial fossa have become well described clinical entities, especially for the fifth and seventh cranial nerves. Jannetta has proposed vascular compression of the eighth nerve as the etiology of hearing loss, tinnitus, and vertigo in some patients. The case that follows illustrates a clear-cut example of vestibular symptoms arising from vascular compression of the eighth nerve. The patient involved had disabling peripheral vertigo refractory to medical management. magnetic resonance imaging documented a tortuous basilar artery compressing the eighth nerve on the involved side. This was confirmed at surgery, and a selective section of the vestibular nerve provided complete relief of disabling symptoms and preservation of hearing. The authors describe the details of this case and the enigma of eighth nerve symptoms due to vascular compression.
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9/13. Vascular loops in internal auditory canal as possible cause of Meniere's disease.

    Vascular loops were found in 2 patients diagnosed clinically as having Meniere's disease. A vascular loop was suspected of being present within the internal auditory canal in another patient who complained of tinnitus and vertigo. diagnosis was performed by air CT cisternography in the former patients and by CT with contrast enhancement in the latter patient. In Case No. 1, the attacks of vertigo disappeared after endolymphatic sac decompression. In Case No. 2, hearing loss progressed despite remission of vertigo. In Case No. 3, the patient had only tinnitus and dizziness. Although it was difficult to definitely conclude that there was a causal relationship between the vascular loop and the clinical symptoms, we felt that there was a need to investigate the vascular loop as a possible cause of vertigo, tinnitus, and progression of sensorineural hearing loss.
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10/13. Auditory and vestibular system findings in patients with vascular loops in the internal auditory canal.

    Many anatomic studies have shown that a loop of the anterior inferior cerebellar artery is frequently found in the cerebellopontine angle and internal auditory canal. The concept of vascular cross-compression has been extended to the eighth cranial nerve, and patients with symptoms of hearing loss, tinnitus, and vertigo have been treated surgically by separating the vascular loop from the nerve. Previous reports have emphasized vascular anatomy, surgical approaches, and treatment results. Our study provides details of audiometric and vestibular system test results in a series of ten patients with prominent vascular loops in the internal auditory canal diagnosed by computerized tomography after subarachnoid space air injection (pneumo-CT). All patients had a unilateral (or asymmetric) hearing loss on the side of the lesion, and no vascular loops were detected on the contralateral sides. Hearing losses ranged from mild to profound. Audiometric findings were generally of a cochlear type, and most patients had excellent speech discrimination. Spontaneous nystagmus was detected in all patients during neurotologic testing, and half of the patients had normal caloric test results. The variability of audiometric and vestibular system test results is probably a reflection of anatomic variations of the vascular loop and its branches. Auditory and vestibular symptoms may be due to a complex interaction between the eighth cranial nerve and the vascular loop, in which the loop compresses the nerve and the nerve compromises circulation to the inner ear. Although symptoms from vascular loops and eighth nerve tumors are similar, the findings of a cochlear type of hearing loss, excellent speech discrimination, and normal caloric test results should raise the suspicion of a vascular loop.(ABSTRACT TRUNCATED AT 250 WORDS)
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