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)

In animals the occurrence of a behavioural syndrome consisting of hyperactivity, stereotyped movements and increase of temperature has been induced by MAOIs, 5-HT precursors (L-tryptophan) and 5-HT reuptake inhibitors. Most of these manifestations were specifically blocked by a pretreatment with an inhibitor of serotonin synthesis. In humans, the association of myoclonus, diarrhea, confusion, hypomania, agitation, hyperreflexia, shivering, incoordination, fever and diaphoresis, when patients are treated with serotoninergic agents, could constitute a "serotonin syndrome". Such cases of serotonin syndrome were reported after treatments with L-tryptophan, MAOIs, serotonin reuptake inhibitors and tricyclics alone or in association. The authors prospectively evaluated all the "serotonin-related" symptoms in 38 depressed inpatients fulfilling DSM III-R criteria of major depression. 16 (42%) out of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously and 10 patients presented at the same time tremor, myoclonus, diaphoresis and shivering. Except for two patients, symptoms were transient, lasted less than one week and disappeared with the pursuit of the treatment. Most often, serotonin syndrome thus corresponds to a reaction induced by a combination of serotoninergic agents at high dosages. In very rare cases, a toxic and potentially fatal interaction can occur between MAOIs, tricyclics and selective serotonin reuptake inhibitors at therapeutic dosages. Serotonin syndrome also provides an heuristic model of the putative mode of action of antidepressants. Serotonin-related symptoms are the physical and objective expression of the antidepressant-induced increase in serotonin. The specificity of serotonin-related syndrome also needs to be discussed since most of the symptoms, such as tremor and diaphoresis, are not in all cases related to an increase in serotonin.
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PMID:[The serotonin syndrome: review of the literature and description of an original study]. 852 62

Seven related Bernese Mountain Dogs developed a syndrome Characterized by progressive cerebellar and hepatic disease. Clinically, stiffness in the hind limbs, mild incoordination, and a slight head tremor were first noticeable when pups were 4 to 6 weeks old. The condition progressed, causing pups to assume a wide-based stance. Other signs included head bobbing, spontaneous nystagmus, and, finally, paresis. Hematologic findings included leukocytosis with a left shift; normocytic, normochromic anemia; hypoproteinemia, low serum creatinine, and urea nitrogen concentrations; excessive fasting plasma ammonia concentration; and an increase in concentration of serum bile acids. Portal venography performed on 1 dog revealed a small liver and extensive extrahepatic varicosities. Necropsy revealed cerebellar hypoplasia, nodular liver, extensive abdominal varicosities, and ascites. Histologically, degeneration and depletion of Purkinje's cells and vacuolation, degeneration, and nodular regeneration of hepatic tissues were evident. Preliminary analysis of the pedigree was suggestive of an autosomal recessive pattern of inheritance.
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PMID:Clinical, hematologic, and biochemical features of a syndrome in Bernese mountain dogs characterized by hepatocerebellar degeneration. 863 71

The current study examined behavioral effects and possible development of physical dependence after once-daily doses of zolpidem (0, 1.0, 3.2, 10.0, 32.0 mg/kg intragastrically [i.g.]) in three baboons. Each dose was administered for 17 days and then the dose was increased; the 32.0 mg/kg dose was administered for 27 days. Baboons had access to food pellets for 20 hr/day beginning 15 min after dosing. Each day, baboons were presented with a fine motor task. Observation sessions were conducted 1 hr after dosing on days 1, 10, 12 and 14 of each dose condition and after termination of drug dosing. On days 10 and 14 of each dose condition, vehicle and flumazenil (5 mg/kg i.m.) were administered, respectively. Zolpidem increased the number of pellets obtained by two of three baboons. Vomit and/or retch and grimace (signs believed to be indicative of abdominal discomfort) were observed in one or two baboons during all zolpidem dose conditions (1.0-32.0 mg/kg). Time to complete the fine motor task increased dose-dependently in all three baboons, and incoordination was observed during the task in two baboons at 10.0 and 32.0 mg/kg. Analysis of blood plasma showed that measurable levels of zolpidem were present 24 hr after dosing in all drug conditions. The signs of flumazenil-precipitated withdrawal were summarized on a 9-point scale. Scores ranged from 1 to 5 in the 1.0 mg/kg condition, from 2 to 5 in the 3.2 and 10.0 mg/kg conditions and from 4 to 6 in the 32.0 mg/kg condition. Signs that were considered intermediate in severity were observed. Specifically, tremor, jerk and/or rigidly braced posture was observed in one baboon at 1.0 mg/kg, two baboons at the next two doses and all three baboons at 32.0 mg/kg. Vomit and/or retch also occurred in two baboons at dose conditions above 1.0 mg/kg. Discontinuation of zolpidem dosing after 78 to 79 days resulted in mild withdrawal signs (e.g., number of pellets obtained were lower and number of 1-min intervals increased in which eyes were closed, or in which lying down, head lower than torso posture and/or withdrawn posture were observed) on the first day in two baboons. The peak withdrawal scores were 4 or 5 on days 5 to 10; two baboons vomited and/or retched and all three baboons showed tremor, jerk and/or rigidly braced posture. Thus, zolpidem produced physical dependence under once-daily dosing conditions, and the severity of the withdrawal syndrome can be characterized as intermediate.
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PMID:Zolpidem physical dependence assessed across increasing doses under a once-daily dosing regimen in baboons. 953 93

Hypoglycemic episodes were studied in two large populations of prepubertal (332 subjects, aged 6-11 years) and adolescent (200 subjects, aged 12-18 years) diabetic children. We confirmed the majority of published data on incidence and causes of hypoglycemia and added some new information on the complex symptomatology and fear of hypoglycemia. Longer duration of IDDM induced a change in the symptomatology of hypoglycemia, consisting of a reduced occurrence of autonomic symptoms, namely tremor, and a parallel increased experience of neuroglycopenic symptoms, particularly drowsiness, difficulty in concentrating, and lack of coordination. The latter symptoms were found more frequently in patients with partial unawareness, more severe episodes and higher fear of hypoglycemia. These observations draw attention to the neuroglycopenic symptoms as important warning cues of hypoglycemia. We emphasized the necessity of observing the change in the frequency of symptoms experienced by patients, in particular autonomic and neuroglycopenic symptoms, in order to educate patients to preserve a normal awareness of hypoglycemia and prevent severe episodes.
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PMID:Problems of hypoglycemia arising in children and adolescents with insulin-dependent diabetes mellitus. The Diabetes Study Group of The Italian Society of Pediatric Endocrinology & Diabetes. 964 56

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
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PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14

An adult white-handed gibbon (Hylobates lar) at a zoo in eastern Kansas was euthanized after developing a head tremor, generalized motor incoordination, and partial paresis of the right arm that persisted over 2 yr. Magnetic resonance imaging early in the course of the disease demonstrated a localized left frontal lobe cerebritis. Larvae morphologically consistent with a Baylisascaris species were seen in tissue sections of the cerebrum and cerebellum. Epizootiologic investigation, which included qualitative fecal flotations, evaluation of soil samples for nematode eggs, and necropsy examination of livetrapped raccoons (Procyon lotor), indicated that Baylisascaris procyonis was most likely to have caused the cerebrospinal nematodiasis in this gibbon.
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PMID:Cerebrospinal nematodiasis in a white-handed gibbon (Hylobates lar) due to Baylisascaris sp. 973 41

We report a case of dystonia with a partial deletion of the short arm (p) of chromosome 18 and androgen insensitivity. Neurologic findings in the 18p syndrome are reported to include mental retardation, seizures, incoordination, tremor, and chorea. A 15-year-old girl with a denovo 18p deletion [karyotype 46, XY, del (18)(p11.1)] developed progressive asymmetric dystonia. She had oromotor apraxia and partial expressive aphasia since childhood, and she was able to partially communicate through elementary sign language. At the age of 15 years, she developed subacute and progressive choreic movements of the right arm, severe dystonic posturing of the left arm, and spastic dystonia in both legs. Her response to parenteral or oral benzodiazepines, oral trihexyphenidyl, benztropine mesylate, baclofen, and L-dopa were brief and inadequate. The response to intrathecal baclofen has been sustained over 18 months. In all likelihood, the 18p deletion syndrome affecting this patient is significant in the pathogenesis of her acquired dystonia. Chronic intrathecal baclofen therapy via pump has been effective in this case and should be considered as a treatment modality in carefully selected patients with dystonia.
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PMID:Progressive dystonia in a child with chromosome 18p deletion, treated with intrathecal baclofen. 1007 26

A late onset of cerebellar degeneration was diagnosed in a one-and-a-half-year-old Siamese cat. The animal had been presented with mild ataxia involving all four limbs. Over the following two years, the signs gradually progressed to severe incoordination, a frequent tendency to fall and a head tremor. The neurological signs were consistent with a diffuse cerebellar lesion and the cat was euthanased. Profound and diffuse Purkinje cell loss was found on histopathological examination, but no aetiological agent was detected.
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PMID:Late onset of cerebellar abiotrophy in a Siamese cat. 1044 56

This report concerns an autopsy case of amyotrophic lateral sclerosis (ALS) with unusual clinical and neuropathological findings. The patient was a Japanese man without hereditary burden who was 49 years old at the time of death. His clinical manifestation included dysarthria at age 48, followed by dysphagia, atrophy and fasciculation of the tongue, muscle weakness in the four extremities, tremor, rigidity, increased deep tendon reflexes in the upper and lower extremities, and incoordination of the four extremities. He died of respiratory failure 12 months after the disease onset. No respirator administration was performed throughout the clinical course. The neuropathological examination revealed not only degeneration of upper and lower motor neuron systems, including the presence of Bunina bodies and ubiquitin-immunoreactive neuronal inclusions in the lower motor neurons, but also prominent degeneration of the substantia nigra and dentate nucleus with slight neuronal loss in the locus ceruleus and pontine nucleus. To our knowledge, this is the first reported case of sporadic ALS without dementia and respirator support, showing degeneration of the substantia nigra and dentate nucleus. This report may contribute to the resolution of the question concerning the neuropathological heterogeneity of sporadic ALS with respiratory support.
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PMID:Sporadic amyotrophic lateral sclerosis with multiple system degeneration: a report of an autopsy case without respirator administration. 1054 75

There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
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PMID:Cerebellar Ataxia. 1109 49


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