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)

Pheochromocytomas classically present with paroxysms of hypertension and adrenergic symptoms including headaches, palpitations, tremor, and anxiety. However, these tumors can be clinically silent and occasionally present only when catecholamine release is up-regulated by exogenous stimuli. In addition, the clinical presentation of pheochromocytoma can mimic a number of more common medical conditions, including migraine headaches, cardiac arrhythmias, and myocardial infarction, making diagnosis difficult. In this report, we present the case of a young woman who, while receiving oral corticosteroid therapy for presumed migraine headaches, suffered a myocardial infarction and ultimately hemorrhaged into a previously undiagnosed pheochromocytoma. Our patient exhibited severe, labile hypertension after the administration of iv beta-blockade for presumed myocardial ischemia, raising our initial clinical suspicion for pheochromocytoma. In this paper we review some of the key clinical issues related to this complex case, including steroid-induced stimulation of catecholamine synthesis and release, the role of pheochromocytoma in myocardial ischemia and electrocardiographic changes, and the rare complication of tumor hemorrhage. We then briefly review the essential diagnostic and management strategies for this rare but potentially lethal tumor, with specific emphasis on pheochromocytoma-related cardiovascular emergencies and the surgical management of tumor hemorrhage.
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PMID:Hemorrhagic pheochromocytoma associated with systemic corticosteroid therapy and presenting as myocardial infarction with severe hypertension. 1591 34

We compared the frequency of migraine among Sydenham's chorea (SC) patients, rheumatic fever (RF) patients without neurological symptoms and matched controls. Migraine was more frequent in SC patients (12/55, 21.8%) than in controls (9/110, 8.1%) and as common as in the RF group (10/55, 18.2%). Our data are in agreement with previous studies reporting higher frequency of migraine in other basal ganglia disorders, such as essential tremor and Tourette's syndrome.
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PMID:Migraine headache in patients with Sydenham's chorea. 1595 42

Brain single photon emission computed tomography (SPECT) studies were conducted in three patients with A3243G mutation of the mitochondrial (mt) DNA tRNA. All were born to mothers suffering from chronic progressive external ophthalmoplegia (CPEO) with the same A3243G point mutation of the mtDNA tRNA. The first case manifested clinically with MELAS, the second case manifested with CPEO, and third case was characterized by recurrent migraine-like headache, tremor, and epilepsy. Brain SPECT of all patients, regardless of whether they had or had not suffered from stroke-like episodes, showed multiple areas of asymmetrical decreased perfusion, particularly in the posterior and lateral head regions, especially the temporal lobes. Crossed-cerebellar diaschisis may occur. Conventional brain magnetic resonance images failed to show some of the lesions. Decreased regional cerebral blood flow, rather than previously proposed hyperemia, is likely to be the cause. We conclude that mitochondrial vasculopathy with regional cerebral hypoperfusion may be seen on brain SPECT in patients with mitochondrial disorders and A3243G mutations, regardless of whether they have or have not suffered from stroke-like episodes.
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PMID:Brain single photon emission computed tomography in patients with A3243G mutation in mitochondrial DNA tRNA. 1596 44

The management of pediatric migraine requires a balance of biobehavioral measures coupled with agents for acute treatment and, if needed, daily preventive medicines. A recent American Academy of Neurology practice parameter has critically reviewed the limited data regarding the efficacy and safety of medicines for the acute and preventive therapy of pediatric migraine. The first step is to establish the headache frequency and degree to which the migraines impact upon lifestyle and performance. The next step is to institute nonpharmacologic measures such as regulation of sleep (improved sleep hygiene), moderation of caffeine, regular exercise, and identification of provocative influences (eg, stress, foods, social pressures). A wide variety of therapeutic options exist for patients whose migraine headaches occur with sufficient frequency and severity to produce functional impairment. The most rigorously studied agents for the acute treatment of migraine are ibuprofen, acetaminophen, and sumatriptan nasal spray, all of which have shown safety and efficacy in controlled trials. Daily preventive drug therapies are warranted in about 20% to 30% of young migraine sufferers. The particular drug selected for the individual patient requires an appreciation of comorbidities such as affective or anxiety disorders, co-existent medical conditions such as asthma or diabetes, and acceptability of potential toxicities such as weight gain, sedation, or tremor.
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PMID:The treatment of pediatric migraine. 1601 27

Antiepileptic drugs (AEDs) affect various neurotransmitters (i.e. GABA, glutamate), receptors (i.e. GABAergic, glutamatergic), and ion channels (i.e. for sodium or calcium) which is responsible for their anticonvulsant activity. However, this broad spectrum of action may be also utilized in other pathological conditions. For example, both conventional and newer AEDs may be used in patients suffering from neuropathic pain, migraine, essential tremor, spasticity, restless legs syndrome and a number of psychiatric disorders (f.e. bipolar disease or schizophrenia). Also, isolated data point to their potential use in Parkinson's or Alzheimer's disease. There is experimental background indicating a potent neuroprotective efficacy of AEDs in numerous models of brain ischemia. However, the clinical data are very limited and this problem requires careful assessment.
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PMID:Non-epilepsy uses of antiepilepsy drugs. 1653 24

The identification of comorbid disorders in migraineurs is important since it may impose therapeutic challenges and limit treatment options. Moreover, the study of comorbidity might lead to improve our knowledge about causes and consequences of migraine. Comorbid neuropathologies in migraine may involve mood disorders (depression, mania, anxiety, panic attacks), epilepsy, essential tremor, stroke, and white matter abnormalities. Particularly, a complex bidirectional relation exists between migraine and stroke, including migraine as a risk factor for cerebral ischemia, migraine caused by cerebral ischemia, migraine as a cause of stroke, migraine mimicking cerebral ischemia, migraine and cerebral ischemia sharing a common cause, and migraine associated with subclinical vascular brain lesions.
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PMID:Comorbid neuropathologies in migraine. 1676 30

Vagus nerve stimulation (VNS) is an established treatment for selected patients with medically refractory seizures. Recent studies suggest that VNS could be potentially useful in the treatment of resistant depressive disorder. Although a surgical procedure is required in order to implant the VNS device, the possibility of a long-term benefit largely free of severe side effects could give VNS a privileged place in the management of resistant depression. In addition, VNS appears to affect pain perception in depressed adults; a possible role of VNS in the treatment of severe refractory headache, intractable chronic migraine and cluster headache has also been suggested. VNS is currently investigated in clinical studies, as a potential treatment for essential tremor, cognitive deficits in Alzheimer's disease, anxiety disorders, and bulimia. Finally, other studies explore the potential use of VNS in the treatment of resistant obesity, addictions, sleep disorders, narcolepsy, coma and memory and learning deficits.
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PMID:Vagus nerve stimulation: indications and limitations. 1769 14

Antiepileptic drugs (AEDs) are used extensively to treat multiple non-epilepsy disorders, both in neurology and psychiatry. This article provides a review of the clinical efficacy of AEDs in non-epilepsy disorders based on recently published preclinical and clinical studies, and attempts to relate this efficacy to the mechanism of action of AEDs and pathophysiological processes associated with the disorders. Some newer indications for AEDs have been established, while others are under investigation. The disorders where AEDs have been demonstrated to be of clinical importance include neurological disorders, such as essential tremor, neuropathic pain and migraine, and psychiatric disorders, including anxiety, schizophrenia and bipolar disorder. Many of the AEDs have various targets of action in the synapse and have several proposed relevant mechanisms of action in epilepsy and in other disorders. Pathophysiological processes disturb neuronal excitability by modulating ion channels, receptors and intracellular signalling pathways, and these are targets for the pharmacological action of various AEDs. Attention is focused on the glutamatergic and GABAergic synapses. In psychiatric conditions such as schizophrenia and bipolar disorder, AEDs such as valproate, carbamazepine and lamotrigine appear to have clear roles based on their effect on intracellular pathways. On the other hand, some AEDs, e.g. topiramate, have efficacy for nonpsychiatric disorders including migraine, possibly by enhancing GABAergic and reducing glutamatergic neurotransmission. AEDs that seem to enhance GABAergic neurotransmission, e.g. tiagabine, valproate, gabapentin and possibly levetiracetam, may have a role in treating neurological disorders such as essential tremor, or anxiety disorders. AEDs with effects on voltage-gated sodium or calcium channels may be advantageous in treating neuropathic pain, e.g. gabapentin, pregabalin, carbamazepine, oxcarbazepine, lamotrigine and valproate. Co-morbid conditions associated with epilepsy, such as mood disorders and migraine, may often respond to treatment with AEDs. Other possible disorders where AEDs may be of clinical importance include cancer, HIV infection, drug and alcohol abuse, and also in neuroprotection. A future challenge is to evaluate the second-generation AEDs in non-epilepsy disorders and to design clinical trials to study their effects in such disorders in paediatric patients. Differentiation between the main mechanisms of action of the AEDs needs more consideration in drug selection for tailored treatment of the various non-epilepsy disorders.
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PMID:Antiepileptic drugs in non-epilepsy disorders: relations between mechanisms of action and clinical efficacy. 1807 13

The role of beta blockers (especially of propranolol, which has been most frequently used) in prophylaxis of migraine and treatment of essential tremor has been evidenced. These are two exceptionally common neurological entities, therefore detailed insight into indications, dose range and side-effects is necessary. Thus, the optimum therapeutical doses of propranolol for prophylaxis of migraine range from 160-240 mg a day, and for treatment of essential tremor from 240-320 mg a day, which, based on our experiences from practice, indicates that a large number of patients is receiving suboptimal doses, being, consequently, devoid of the best therapeutical effect.
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PMID:[Beta blockers in the treatment of neurological disorders]. 1819 12

This was a double-blind clinical trial designed to assess the efficacy and safety of the cinnarizine (CIN) in patients with migraine who were refractory to propranolol and tricyclic antidepressants in comparison with sodium valproate (SV) to investigate whether CIN could be at least as effective as SV. A total of 125 patients were treated in a treatment period of 12 weeks. All patients had at least one intake of trial medication and 2-week post baseline efficacy observation which all were included in the ITT analysis. Of the 125 subjects treated, 46 discontinued prematurely: 25 from the CIN and 21 from the SV group. The main reasons for premature discontinuation were: lost to follow up (25/46, 63.2%), insufficient response (16/46, 20%), and adverse events (5/46, 12.8%). No statistically significant inter-group differences in the number of discontinuation was observed (p > 0.05). In both groups, number of attacks, intensity, and duration of attacks significantly decreased (p < 0.05). No statistically significant inter-group differences were observed regarding the mean number of attacks, duration, and intensity of migraine attacks for any of the time intervals analysed, except for the mean reduction of third and fourth visits intensity from baseline which were significantly different in two groups (p < 0.05), with the CIN group showing more reduction. Analysis of the number of responders showed that in the CIN group 61.2% subjects were responders, and 63.8% in the SV group. No statistically significant differences between the treatment groups were found for any of the secondary parameters. Overall 26 subjects reported one or more adverse events during the study period: 13 subjects in each group. Five subjects discontinued prematurely due to adverse events; two in the CIN group with significant weight gain, and 3 in the SV group with significant weight gain and severe tremor. These results suggest that CIN is an effective and safe prophylactic agent even in severe migraine headache.
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PMID:Cinnarizine in refractory migraine prophylaxis: efficacy and tolerability. A comparison with sodium valproate. 1828 31


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