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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Palatal tremor (formerly palatal myoclonus) is an extremely rare, but potentially treatable cause, of objective tinnitus. The tinnitus is thought to be secondary to rhythmic involuntary movements of the soft palate. Its aetiology is variable and it remains difficult to treat. Many different medical and surgical remedies have been tried but none have demonstrated reproducible success. Botulinum toxin has been used in sporadic cases and seems to produce good results. Ten patients with palatal tremor have presented to this department over the last three years. After discussion with the patients with regard to the management of this condition and possible complications, five opted for botulinum toxin therapy and five declined further intervention. Clinical diagnosis was made on the confirmation of soft palate movements synchronous with an audible clicking noise. Five patients underwent botulinum toxin injection into the insertion of the levator and tensor veli palatini muscles. Of the five that were treated with toxin, four showed complete resolution of symptoms after a course of treatment. Only one patient reported transient side effects. This would suggest that botulinum toxin is a safe and effective first line treatment for palatal tremor.
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PMID:Botulinum toxin is effective and safe for palatal tremor: a report of five cases and a review of the literature. 1684 71

A healthy 5-year-old male reported a clicking sound in both ears. Neurologic examination was normal except for an audible clicking noise that could be heard when within 10 cm of either ear and bilateral rapid rhythmic movements of the soft palate. All tests were normal including magnetic resonance imaging brain scan. One year after onset, his objective tinnitus and palatal tremor were no longer present.
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PMID:Objective tinnitus due to essential palatal tremor in a 5-year-old. 1735 51

Palatal tremor is a rare neurotological disorder responsible for objective tinnitus in children. Palatal tremor may be symptomatic of an underlying neurological disease or essential when a cause cannot be identified. We report a case of an essential palatal tremor in a 10-year-old girl complaining of clicking tinnitus. No treatment was undergone as she was not obviously bothered by the ear-clicking sound. Different treatment modalities have been used for distressing tinnitus related to palatal myoclonus. Recently several publications reported satisfactory results with botulinum toxin injection, which seems to be the treatment of choice.
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PMID:[Objective tinnitus and essential palatal tremor in children: report of a case]. 1981 74

The Bible, a major pillar of Western Civilization consists of Hebrew Scriptures, assembled over a millennium and accepted as of divine origin. The Talmud is a compendium of Jewish laws, covering every possible aspect of life, analyzed in depth from 200 BCE to 600 CE, becoming the foundation of Jewish existence. The all-encompassing character of the books provides numerous medical problems and observations that appear in various connotations. When in need to clarify various legal dilemmas, the Talmudic sages displayed astoundingly accurate anatomical knowledge and were pioneers in clinical-pathological correlations. The descriptions of "neurological" events in the Bible are very precise but show no evidence of neurological knowledge. Those reported in the various tractates of the Talmud are evidence of a substantial medical knowledge, marked by Hellenistic influence. Subjects such as head and spinal injuries, epilepsy, handedness neuralgias aphasia tinnitus and tremor were discussed in depth. This chapter is an updated collection of the studies, extracting observations and discussions of neurological manifestations from the ancient texts.
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PMID:Chapter 4: neurology in the Bible and the Talmud. 1989 7

Tinnitus is an auditory disorder characterized by perception of internally generated phantom auditory sensations without corresponding mechanical stimuli arising from the body or external environment. Current auditory based treatment approaches, sometimes in conjunction with nonauditory based strategies, such as Tinnitus Retraining Therapy and Cognitive Behavioral Therapy, have been helpful in mitigating symptoms for the majority of patients. Yet there are over 1 million tinnitus sufferers who still endure troublesome chronic, continuous head noises that are debilitating and interfere with activities of daily living. Here we show that application of deep brain stimulation (DBS) therapy to a locus of caudate neurons (area LC) in the body of the nucleus, a subsite of the striatum that is not part of the classical auditory pathway, can decrease or increase tinnitus loudness perception. The DBS lead traversed through or was adjacent to area LC in six Parkinson's disease and essential tremor subjects with concomitant tinnitus who underwent implantation of the subthalamic or ventral intermediate nucleus. In five subjects where the DBS lead tip traversed area LC, tinnitus loudness in both ears was suppressed to a nadir of level 2 or lower on a 0-10 rating scale. In one subject where the DBS lead was outside area LC, tinnitus was not modulated. In three subjects with preoperative and postoperative audiograms, hearing thresholds were unchanged by area LC stimulation. Neuromodulation of area LC may be interrupting perceptual integration of phantom sensations generated in the central auditory system. This new, basal ganglia based approach to tinnitus modulation warrants further investigation and may be ultimately refined to treat patients with refractory symptoms.
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PMID:Tinnitus modulation by deep brain stimulation in locus of caudate neurons (area LC). 2054 95

MoM hip bearings are being scrutinized due to high early failure rates and concerns that the results of the revision surgeries will be poor. However, orthopedic surgeons and the general medical community are unaware that patients with MoM bearings are also at risk for cobaltism. Medical providers need to know that hip arthroplasty implantees that present with symptom complexes that include tinnitus, deafness, vertigo, visual changes, rashes, hypothyroidism, tremor, dyspnea on exertion, mood disorders, dementia, heart failure, and peripheral neuropathy may be presenting arthroprosthetic cobaltism. These patients need to be asked if they have had a hip replacement and if so what type. For those patients implanted with a MoM bearing or those with a history of hip revision for a failed ceramic bearing obtaining a [Co] is indicated. MoM implantees with renal failure are a particularly high risk for cobaltism. A [Co] can be measured by many reference laboratories from royal blue top trace elements tube of venous blood. Venipuncture with a standard needle is adequate as long as a red stoppered tube is drawn first. The radiographic appearance of a MoM bearing is readily apparent to an orthopedic surgeon. The patient's operative report will usually specify the bearing type. Given that the publicity of the recent ASR bearing recall medical providers will be contacted by worried patients concerned about their hip implants. Most patients with hip replacements will not know the brand or material of their bearings. Providing patients with copies of their hip implant inventory might avoid worry by the majority of patients with hip arthroplasties that are not at risk. Patients with a cobalt levels of greater than 7 mcg/l bear observation of neurologic and cardiac function. Those patients with levels greater than 20 should be advised to have revision of their hip arthroplasty to a bearing that eliminates cobalt. Most patients implanted with MoM bearing have cobalt levels greater than those allowed in industry and cobalt exposed workers may have an increased incidence of subclinical cognitive and cardiac impairments. This association merits further study. Table 1 is a summation of the previously referenced data of this paper that might assist the clinician in interpreting a [Co].
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PMID:Arthroprosthetic cobaltism: identification of the at-risk patient. 2106 26

Cobalt exerts well-known and documented toxic effects on the thyroid, heart and the haematopoietic system, in addition to the occupational lung disease, allergic manifestations and a probably carcinogenic action. Cobalt neurotoxicity is reported in isolated cases, and it has never been systematically treated. Bilateral optic atrophy and retinopathy, bilateral nerve deafness and sensory-motor polyneuropathy have been described long ago as a result of chronic occupational exposure to cobal powder or during long-term treatment of anaemia with cobalt chloride. Recently, some patients with high levels of cobalt released from metal prosthesis have been referred as presenting with tinnitus, deafness, vertigo, visual changes, optic atrophy, tremor and peripheral neuropathy. The aim of this work is to group these cases and to identify a possible mechanism of cobalt neurotoxicity, focusing on hypothetic individual susceptibility such as altered metal-binding proteins, altered transport processes in target cells or polymorphic variation of genetic background.
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PMID:Neurotoxicity of cobalt. 2172 76

The 1.4Mb tandem-duplication in the PMP22 gene at 17p11.2 usually manifests as hereditary sensorimotor polyneuropathy with foot deformity, sensorineural hearing-loss, moderate developmental delay, and gait disturbance. Hypertelorism and marked phenotypic variability within a single family has not been reported. In a single family, the PMP22 tandem-duplication manifested as short stature, sensorimotor polyneuropathy, tremor, ataxia, sensorineural hearing-loss, and hypothyroidism in the 27 years-old index case, as mild facial dysmorphism, muscle cramps, tinnitus, intention tremor, bradydiadochokinesia, and sensorimotor polyneuropathy in the 31 year-old half-brother of the index-patient, and as sensorimotor polyneuropathy and foot-deformity in the father of the two. The half-brother additionally presented with hypertelorism, not previously reported in PMP22 tandem-duplication carriers. The presented cases show that the tandem-duplication 17p11.2 may present with marked intra-familial phenotype variability and that mild facial dysmorphism with stuck-out ears and hypertelorism may be a rare phenotypic feature of this mutation. The causal relation between facial dysmorphism and the PMP22 tandem-duplication, however, remains speculative.
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PMID:Hypertelorism in Charcot-Marie-Tooth disease 1A from the common PMP22 duplication: A Case Report. 2249 45

Palatal tremor is a rare movement disorder characterized by rhythmic movement of the soft palate. There are two subtypes: essential and symptomatic palatal tremor. Essential palatal tremor is characterized by tinnitus and an absence of other neurological deficits. Different treatment options have been used to treat palatal tremor, with varying success rates. Here we describe a patient with essential palatal tremor and who was treated with botulinum toxin injections.
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PMID:Essential palatal tremor treated with botulinum toxin. 2358 64

Symptomatic palatal tremor is potentially the result of a lesion in the triangle of Guillain-Mollaret (1931) and is associated with hypertrophic olivary degeneration (HOD) which has characteristic MR findings. The triangle is defined by dentate efferents ascending through the superior cerebellar peduncle and crossing in the decussation of the brachium conjunctivum inferior to the red nucleus, to finaliy reach the inferior olivary nucleus (ION) via the central tegmental tract. The triangle is completed by ION decussating efferents terminating on the original dentate nucleus via the inferior cerebellar peduncle. We can demonstrate the anatomy of this anatomical triangle using a clinical case of palatal tremor presenting with bilateral subjective pulsatile tinnitus along with the pathognomonic MR findings previously described. The hyperintense T2 signal in these patients may be permanent, but the hypertrophied olive normally regresses after 4 years. The temporal relationship between the evolution of the histopathology and the development of the palatal tremor remains unknown as does the natural history of the tremor. Botox injection at the level of tensor and levator veli palatini insertion have been used to treat patients with disabling tremor synchronous tinnitus. A lesion involving the triangle can have a quite varied clinical expression.
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PMID:The dentato-rubro-olivary tract: clinical dimension of this anatomical pathway. 2366 32


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