Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As dizziness can be caused by so many different pathophysiological mechanisms, it is crucial to determine the type of dizziness before proceeding with the diagnostic evaluation. Vertigo, defined as an illusion of movement, is an important subtype of dizziness that indicates a lesion somewhere within the vestibular system. Probably the most useful feature for differentiating between peripheral and central causes of vertigo is the associated symptoms. Vertigo of peripheral origin is typically associated with auditory symptoms such as hearing loss and tinnitus, while vertigo of central origin is nearly always associated with neurological symptoms such as diplopia, weakness, numbness and ataxia. Each of the common causes of vertigo has a characteristic clinical profile that should suggest a likely diagnosis after the history and examination are complete. Probably the most important treatment breakthrough is the positional manoeuvre that reliably cures benign positional vertigo (see Chapter 6). The treatment strategy for an acute peripheral vestibular lesion has evolved over the past few years. Patients are encouraged to return to normal physical activity as rapidly as possible. Repeated head, eye and body movements (vestibular rehabilitation) help the brain to recalibrate the relationship between visual, proprioceptive and vestibular signals (Chapter 9).
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PMID:Approach to the dizzy patient. 787 2

We describe a patient with a liver abscess due to Entamoeba histolytica, in whom metronidazole therapy (total dose, 21 g over 14 days) was complicated by reversible deafness, tinnitus, and ataxia and who relapsed 5 months later with a splenic abscess. Two courses of tinidazole (the second in combination with percutaneous aspiration of the abscess) were required to achieve cure.
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PMID:Amebic abscess of the spleen complicated by metronidazole-induced neurotoxicity: case report. 798 15

A case of cavernous angioma of the pons which was surgically and successfully excised was reported. A 36 year-old man complained of progressive headache, double vision and tinnitus. Neurologic examination revealed left fifth, sixth and seventh cranial nerve palsies. He had left limb ataxia and right sided hemisensory deficit. A computed tomographic (CT) scan on admission disclosed a hematoma in the left lateral portion of the pons. Serial CT scans demonstrated progressive increase of hematoma. MRI scans revealed an area of mixed signal intensity in T1 weighted images. These findings were thought to be consistent with a cavernous angioma. Three months after the onset, surgery was performed using a lateral suboccipital approach. Histological examination disclosed cavernous angioma. After surgery, the patient's neurological deficits improved, and after 3 months, all symptoms except the mild limb ataxia had disappeared.
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PMID:[Surgical removal of lateral pontine cavernous angioma: review of the surgically treated cases in the literature]. 842 94

The results from 100 patients with 103 acoustic neurinomas who were operated on between February 1979 and April 1992 are presented. All patients were placed in the half-sitting position and operated on by the same surgeon using the suboccipital-trans-meatal approach. Postoperative facial nerve function was good in 56%, moderate in 20% and poor in 24% of our patients. Preservation of useful hearing was achieved in 21%: the smaller the tumor, the better the functional result. However, the early symptoms of acoustic neuromas (tinnitus, dizziness, feeling of unsteadiness) were only slightly improved by the operation. The result concerning tinnitus seemed to be better after sacrificing the cochlear nerve. The number of patients with ataxia increased postoperatively, although objective ataxia decreased. Dizziness improved regardless of the tumor size.
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PMID:[Results of 100 consecutively operated patients with acoustic neuroma]. 850 11

Since the discovery of the biologically active platinum complexes 30 years ago, 2 agents have become widely established in clinical oncology practice. Both cisplatin and carboplatin are platinum(II) complexes with 2 ammonia groups in the cis- position. However, they differ in their solubility, chemical reactivity, dichloride or alicyclic oxygenated leaving groups, pharmacokinetics and toxicology. Cisplatin causes severe renal tubular damage and reduces glomerular filtration, and requires concurrent saline hydration and mannitol diuresis to eliminate potentially lethal and unacceptable damage to the kidneys. Carboplatin, at conventional doses, causes no decrease in glomerular filtration and only minor transient elevations in urinary enzymes. Cisplatin is the most emetic cancer drug in common use, while nausea and vomiting associated with carboplatin are moderately severe. Serotonin release from enterochromaffin gut mucosal cells and stimulation of serotonin 5-HT3-receptors mediates acute emesis. Selective inhibitors of the 5-HT3-receptor protect against cisplatin- and carboplatin-induced nausea and vomiting. Peripheral neurotoxicity is the most dose-limiting problem associated with cisplatin. Loss of vibration sense, paraesthesia and sensory ataxia comes on after several treatment cycles. Carboplatin, however, is relatively free from peripheral neurotoxicity. Audiometry shows cisplatin-induced ototoxicity in 75 to 100% of patients, which may be associated with tinnitus and hearing loss. Ototoxicity is rare with conventional dose carboplatin therapy. Monitoring hearing with audiograms may identify early signs before significant impairment occurs. Cisplatin causes mild haematological toxicity to all 3 blood lineages. Haematological toxicity is dose-limiting for carboplatin, with thrombocytopenia being a greater problem than leucopenia. Although carboplatin is not toxic to the kidney, renal function markedly affects the severity of carboplatin-induced thrombocytopenia. The major clearance mechanism of cisplatin is irreversible binding in plasma and tissues, while carboplatin is cleared by glomerular filtration. Metabolism of cisplatin to aqua, amino acid and protein species is extensive, whereas carboplatin exists mainly as the free unchanged form. Strong relationships between carboplatin renal clearance, glomerular filtration rate, area under the plasma concentration-time curve (AUC) of filterable platinum and severity of thrombocytopenia have prompted dose adjustment according to renal function. New analogues such as JM216 offer the potential advantages of oral administration and few nonhaematological toxicities. Analogues based on the diaminocyclohexane ligand have encountered problematic neurotoxicity.
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PMID:Comparative adverse effect profiles of platinum drugs. 857 96

Cogan's syndrome is an idiopathic inflammatory disease which may present as interstitial keratitis, inflammation of other ocular structures, Meniere's-like attacks, or systemic vasculitis. Although the ocular manifestations respond to topical steroids and are rarely serious, permanent deafness may result if systemic steroid therapy is not promptly instituted for audiovestibular dysfunction, while major morbidity and even death may occur if systemic sequelae such as vasculitis and aortic insufficiency are not recognized. For these reasons, ophthalmologists must suspect Cogan's syndrome in any patient presenting with ocular inflammation who develops hearing loss, vertigo, ataxia, tinnitus, systemic vasculitis, or aortic insufficiency.
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PMID:Cogan's syndrome: ophthalmic, audiovestibular, and systemic manifestations and therapy. 877 69

The term "vestibulocerebellar ataxia" has been applied to a rare, autosomal dominant, late-onset disease with unusual ocular motility findings. We examined the ocular motility of 18 family members from two different kindreds and found 11 affected individuals. Both families in the present study, one of which was originally described by Farmer and Mustian, as well as the family reported by Farris et al., originated from Johnston County, North Carolina. We suspect that all three of these families have a common ancestral origin. The age of onset of the disorder was 31-60 years in the individuals examined. Ataxia, vertigo, diplopia, oscillopsia, and tinnitus were common complaints. Although a variety of eye movement abnormalities have previously been described in this disease, the most prominent and consistent findings in our patients were (a) abnormal smooth pursuits, (b) inability to suppress the vestibuloocular reflex (VOR), and (c) gaze-evoked nystagmus. These findings suggest that the cerebellar flocculus may be the primary site of pathology.
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PMID:Ocular motility in North Carolina autosomal dominant ataxia. 879 63

Immune-mediated inner ear disease, first described by McCabe in 1979, typically presents with an idiopathic, rapidly progressive bilateral sensorineural hearing loss. The course of the hearing loss occurs over weeks to months. It may occur in both sexes and at a variety of ages, but is most common in middle-aged females. It may be accompanied by tinnitus, Meniere's-like vertigo, or more commonly, ataxia or unsteadiness. Approximately 30% of patients will have associated systemic immune-mediated disease. Although refinements in laboratory tests for specific inner ear antigens are being made, and non-specific laboratory indicators of inflammatory or systemic immune disease may be useful in confirming the diagnosis, the most important diagnostic finding is the improvement in hearing seen with a trial of immunosuppressants. This report includes a typical evaluation of the patient with suspected immune-mediated inner ear disease and an illustrative case. Sensorineural hearing loss due to immune-mediated inner ear disease, although unusual as a cause of hearing loss, is important to recognize because early diagnosis and treatment can have a marked effect on the clinical outcome.
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PMID:Clinical evaluation and treatment of immune-mediated inner ear disease. 893 29

Sensorineural hearing loss, tinnitus, dizziness and ataxia are recognised symptoms associated with Chiari malformations but they are rarely the presenting complaints. Patients with such symptoms are frequently referred to otolaryngologists and audiological physicians. We report a case of a 13-year-old girl who presented complaining of tinnitus and impaired hearing, and was subsequently diagnosed as having a type I Chiari malformation. Pure tone audiogram showed a mild hearing impairment on the left side and the speech audiogram was normal. Auditory brain stem responses and the electronystagmography were abnormal. The patient underwent posterior fossa decompression following which her tinnitus disappeared, the hearing problem recovered and some of the abnormal electrophysiological parameters were corrected.
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PMID:Audio-vestibular manifestations of Chiari malformation and outcome of surgical decompression: a case report. 894 83

A 44 year old woman presented with frequent paroxysms of unilateral tinnitus and ataxia which were abolished by treatment with carbamazepine. Hearing was normal and initially there were no other symptoms or signs between paroxysms. Brain stem evoked responses from the affected left ear were absent and MRI showed a large tumour in the left cerebellopontine angle. This was completely removed and histologically proved to be a meningioma. There were striking similarities to trigeminal neuralgia and other paroxysmal brain stem symptoms which occasionally occur in multiple sclerosis and diseases of the cerebellopontine angle. Possible mechanisms are discussed.
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PMID:Paroxysmal tinnitus due to a meningioma in the cerebellopontine angle. 912 Apr 61


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