Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Flunarizine (FZ) is a selective calcium channel blocker used in the therapy of migraine and vertigo. FZ and its parent compound cynnarizine (CZ), may cause movement disorders similar to those observed with neuroleptics, including orofacial dyskinesia, Parkinsonism and postural tremor. A recent report showed that the FZ improves essential tremor (ET); therefore we studied the effects of FZ in 12 patients with moderate to severe ET. Tremor was evaluated after 8 weeks of treatment and was assessed in relation to disability in areas of dressing, writing, eating and drinking. FZ was initially administrated in a dose of 5 mg, in the evening, and after ten days it was increased to 10 mg, and continued for a 7 week period. No changes were made in concurrent medications during the study. It was observed that FZ is an ineffective drug in moderate to severe ET and may worsen the symptoms in some patients. The results of our study exclude the use of FZ in the treatment of ET, especially in elderly patients.
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PMID:Flunarizine and essential tremor in the elderly. 1865 12

Zonisamide (ZNS), a sulfonamide antiepileptic drug, is indicated as an adjunct therapy for partial seizure disorders with and without secondary generalization. ZNS has a favorable pharmacokinetic profile because of its rapid absorption and high bioavailability. Its activity is related to the blockade of voltage gated sodium and calcium channels, modulation of central dopaminergic, GABAergic, and serotonergic functions, as well as inhibition of carbonic anhydrase and monoamine oxidase B. ZNS has potential efficacy for an array of neuropsychiatric disorders including migraine and other headache syndromes, neuropathic pain, Parkinson's disease, essential tremor, stroke, obesity, anxiety, bipolar and binge-eating disorders.
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PMID:Therapeutic role of zonisamide in neuropsychiatric disorders. 1878 51

The antiepileptic agent topiramate has proved its efficacy in a variety of other conditions as well, including several kinds of tremor and migraine prophylaxis. We report on the case of a 42-year-old depressive female patient with comorbid migraine attacks, whereby the adjunction of topiramate as an antimigraine agent at the dosage of 50 mg/d to her antidepressive treatment with fluvoxamine at 300 mg/d triggered--the prima facie paradoxical for topiramate--side effects of tremor and myoclonus. Topiramate was immediately discontinued, and patient's abnormal movements subsided completely within 24 to 72 hours. Topiramate was possibly the cause of patient's abnormal movements enhanced by fluvoxamine's potential to induce also tremor and myoclonus. Therefore, clinicians should be aware of the potentially severe adverse reactions that might occur during concomitant treatment with fluvoxamine and topiramate.
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PMID:Reversible tremor and myoclonus associated with topiramate-fluvoxamine coadministration. 1905 Apr 15

The "new" antiepileptic drug levetiracetam has the unique mechanisms of antiepileptic activity. Various recent studies revealed its efficacy and safety in different forms of epilepsy both as a monotherapy and an additional therapy. The low frequency of side-effects and minimal interactions with other drugs allow to use levetiracetam in elderly patients and in patients with severe co-morbid diseases including AIDS and hepatitis C receiving the corresponding therapy. Moreover, the efficacy of levetiracepam in other neurological diseases: chronic headaches, i.e., migraine, neuropathic pain, including patients with cancer, movement disorders (myoclonus, dystonia and dyskinesia in Parkinson's disease, essential tremor, have been revealed.
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PMID:[The possibilities of using keppra (levetiracetam) in different neurological diseases]. 1943 Dec 51

Neuropathic pain is a phenomenon characterized by a high population prevalence by possessing several etiologies. In contrast to nociceptive pain, painful signals in neuropathic pain are originated in the nervous system, present poor responses to conventional treatments and may worsen the quality of life. Antiepileptic drugs are increasingly used for different purposes including migraine, neuropathic pain, tremor or psychiatric disorders and they have started to be called neuromodulators. These drugs may act on very different targets such as sodium, potassium or calcium channels, purinergic, GABAergic, glutamatergic or vanilloid receptors and different cytokines including IL-6 or TNF, each if which may be important in managing some aspects of neuropathic pain. Antiepileptic drugs have demonstrated effectiveness in the treatment of this pathology, and owing to the important development of these drugs in the last years, they may become a very effective tool. On the other hand, the increasing knowledge of the pathophysiology of nociception is leading to new channels and receptors as potential targets for treatment. In this paper we try to review the different potential therapeutic targets and role of antiepileptic drugs in the treatment of this pathology.
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PMID:Neuromodulators and therapeutic targets in neuropathic pain: from molecules to man. 1960 15

Divalproex (DVP) delayed release and DVP extended release (DVP ER) are approved by the Food and Drug Administration for bipolar disorder, epilepsy, and migraine prophylaxis. Divalproex ER is given once daily, improving compliance and reducing adverse events. Overnight switch to DVP ER is advised in the package insert but could produce more adverse events in this susceptible population. In this pilot study, we compared tolerability of overnight versus gradual switching to DVP ER in 16 adults with intellectual and developmental disabilities receiving DVP, in 9 for epilepsy and in all 16 for comorbid bipolar disorder. The study design was open with parallel groups. Sixteen subjects with intellectual and developmental disabilities were randomized to overnight or gradual conversion for 4 to 6 days. A blinded rater completed the Multidimensional Observation Scale for Elderly Subjects on days +1, +4, and +8 after the switch began. We found no major differences between the 2 groups at each time point. Neither group of subjects, except for 1 subject in the overnight group, manifested sedation, seizures, worsening of tremor, or gastrointestinal adverse events. One subject in the overnight group manifested acute diarrhea and vomiting, followed by a very brief tonic leg seizure 6 days later. Larger studies are warranted.
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PMID:Overnight versus progressive conversion of multiple daily-dose divalproex to once-daily divalproex extended release: which strategy is better tolerated by adults with intellectual disabilities? 1974 51

The mechanisms of vestibular migraine and motion sickness remain unknown. The aims of this study were to determine interictal vestibular dysfunction in migraineurs according to associated dizziness/vertigo and motion sickness, and to find out whether impaired uvulonodular inhibition over the vestibular system underlies the vestibular symptoms and signs by measuring tilt suppression of the vestibulo-ocular reflex (VOR). One hundred and thirty-one patients with migraine [65 with vestibular migraine (MV), 41 with migrainous dizziness (MD), and 25 with migraine only (MO)] and 50 normal controls underwent evaluation of vestibular function. Motion sickness was assessed using the motion sickness susceptibility questionnaire (MSSQ) and subjective scale. Compared with normal controls and MO group, patients with MV/MD showed increased VOR time constant (TC) and greater suppression of the post-rotatory nystagmus with forward head tilt. The mean MSSQ score and subjective scale were highest in MV group, followed by MD, MO, and controls (p = 0.002, p < 0.001). Multiple linear regression model analyses revealed that motion sickness is an independent factor of TC prolongation (p = 0.024). Twenty-eight (21.4%) patients with migraine also showed perverted head shaking nystagmus and 12 (9.2%) had positional nystagmus. In view of the increased tilt suppression of the VOR, we speculate that dysfunction of the nodulus/uvula may not account for the prolonged TCs in MD/MV. Instead, innate hypersensitivity of the vestibular system may be an underlying mechanism of motion sickness and increased TC in MD/MV. The increased tilt suppression may be an adaptive cerebellar mechanism to suppress the hyperactive vestibular system in migraineurs.
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PMID:Vestibular dysfunction in migraine: effects of associated vertigo and motion sickness. 2004 31

Essential tremor (ET) and migraine headache are considered comorbid diseases on the basis of uncontrolled studies. We investigated the frequency of migraine in patients with ET by enrolling 110 patients with ET and 110 age- and sex-matched healthy controls in a case-control study. We found no significant differences in the frequency of lifetime and current migraine between patients and controls, even in patients stratified for age. Tremor had similar clinical features in patients with ET with and without migraine except that females predominated in patients with ET and migraine. Migraine also had similar characteristics in both patients with ET and migraine and in controls with migraine. Our study excludes a comorbid association between ET and migraine. When ET and migraine coexist their clinical phenotype and evolution remain almost unchanged.
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PMID:No association between essential tremor and migraine: a case-control study. 2051 Dec 7

Friedrich Nietzsche developed dementia at the age of 44 years. It is generally assumed that the cause of his dementia was neurosyphilis or general pareisis of the insane (GPI). Others have proposed frontal-based meningioma as the underlying cause. We have reviewed Nietzsche's medical history and evaluated the evidence from the medical examinations he underwent by various physicians. We have viewed the possible diagnosis of GPI or meningioma in light of present neuro-ophthalmic understanding and found that Nietzsche did not have the neurological or neuro-ophthalmic symptoms consistent with a diagnosis of GPI. The anisocoria which was assumed to be Argyll Robertson pupil was present since he was six years of age. He did not have tongue tremor, lacked progressive motor features and lived at least 12 years following the onset of his neurological signs. Furthermore, the headaches that have been attributed to a frontal-based tumour were present since childhood and the pupil abnormality that has been interpreted as an "afferent pupillary defect" had the characteristics of an abnormality of the efferent pupillary innervation. None of the medical records or photographs suggest there was any ocular misalignment. We concluded that neither diagnosis of GPI nor frontal-based meningioma is convincing. It is likely that Nietzsche suffered from migraines, his blindness in his right eye was a consequence of high progressive myopia associated with retinal degeneration, his anisocoria explained by unilateral tonic pupil, and his dementia by an underlying psychiatric disease.
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PMID:Friederich Nietzsche and the seduction of Occam's razor. 2054 32

Although zonisamide was previously only used to treat epilepsy, recently more applications have been forthcoming. Due to a good side effect profile, a lower frequency of interactions and a more comfortable posology, there are several studies regarding its uses in other pathologies such as migraine, neuropathic pain, essential tremor and various psychiatric diseases. A multicentered, randomized, double-blind, placebo-controlled study conducted in Japan suggested that zonisamide, as an add-on treatment, has efficacy in treating motor symptoms in patients with Parkinson's disease. In addition, other studies support the utility of zonisamide in other symptoms of this disease. The therapeutic doses of zonisamide for the treatment of Parkinson's disease are considerably lower than those for the treatment of epilepsy. This antiepileptic drug has been used in Japan for more than 15 years and so it is expected that it will be safe and well tolerated in patients with Parkinson's disease. However, the pharmacological mechanisms of the antiparkinsonian actions of zonisamide remain unclear and more basic investigation is warranted. The aim of this paper is to review the structure, mechanisms of action, pharmacokinetics and antiparkinsonian action of zonisamide.
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PMID:A review of the use of zonisamide in Parkinson's disease. 2118 Jun 21


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