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Ataxias

Benzodiazepines. Several BZs have anticonvulsant activity and ate used for the treatment of epilepsy producing their anticonvulsant actions via interactions with the GABA /BZ receptor complex to enhance inhibitory GABAergic transmission (1). The anticonvulsant actions of the BZs tend to tolerate upon chronic usage in six months, and BZs also lead to withdrawal symptomatology. Other side effects include sedation, ataxia, and cognitive impairment. [Pg.535]

Other agents are also used for the treatment of manic-depressive disorders based on preliminary clinical results (177). The antiepileptic carbamazepine [298-46-4] has been reported in some clinical studies to be therapeutically beneficial in mild-to-moderate manic depression. Carbamazepine treatment is used especially in bipolar patients intolerant to lithium or nonresponders. A majority of Hthium-resistant, rapidly cycling manic-depressive patients were reported in one study to improve on carbamazepine (178). Carbamazepine blocks noradrenaline reuptake and inhibits noradrenaline exocytosis. The main adverse events are those found commonly with antiepileptics, ie, vigilance problems, nystagmus, ataxia, and anemia, in addition to nausea, diarrhea, or constipation. Carbamazepine can be used in combination with lithium. Several clinical studies report that the calcium channel blocker verapamil [52-53-9] registered for angina pectoris and supraventricular arrhythmias, may also be effective in the treatment of acute mania. Its use as a mood stabilizer may be unrelated to its calcium-blocking properties. Verapamil also decreases the activity of several neurotransmitters. Severe manic depression is often treated with antipsychotics or benzodiazepine anxiolytics. [Pg.233]

Rats exposed to 1000 ppm of vapors for 4—7 h/d for eight days showed ataxia, decreased body weight and growth rate, and minimal central fatty metamorphosis of the Hver (119). Trichloroethanol and trichloroacetic acid were urinary metaboHtes. Tetrachloroethylene did not show any of these effects. [Pg.13]

White has shown that the lysergic acids themselves exhibit weakly some, but not all, of the types of activity characteristic of the alkaloids of higher molecular weight. Both acids produce a slight transitory cyanosis of the cockscomb and cause ataxia and delayed miosis in the cat and also relax the isolated rabbit intestine. On the whole, lysergic acid appeared more active than the isomeride. [Pg.534]

Angrcecum fragrans. Myroxylon Pereira. Cevatopetalum apetalum. Ataxia Horsfeldii. [Pg.272]

Antiepileptics Na+, Ca2+ channels GABA receptors l Na+currents l Ca2+ currents GABA receptor activity l Excitability of peripheral and central neurons l Release of excitatory neurotransmitters Sedation, dizziness, cognitive impairment, ataxia, hepatotoxicity, thrombocytopenia... [Pg.76]

Episodic ataxia (EA) is an autosomal dominant disorder that brief episodes of ataxia can be triggered by physical or emotional stress. The symptom can occur several times during the day, last for seconds to minutes, and be associated with dysarthria and motor neuron activity, which causes muscle rippling (myokymia) between and during attacks. It is caused by a mutation in a neuronal voltage dependent Ca2+ channel. [Pg.479]

VLDL receptor Loss-of-function (familial, autosomal recessive) Autosomal recessive cerebellar hypoplasia (ataxia, mental retardation)... [Pg.706]

Mutation in the neuronal Cav2.1 channel is associated with familial hemiplegic migraine and episodic ataxia in humans. Deletion of the Cav2.1, Cav2.2 and Cav2.3 gene is compatible with life accompanied by a variety of central and peripheral defects. [Pg.1304]

EA, episodic ataxia LQT, long QT syndrome JLN, Jervell-Lange Nielsen syndrome BFNC, benign familial epilepsy DFNB2, deafness syndrome... [Pg.1312]

Mutations in human Kv-channel genes have been detected that are associated with hereditary diseases ranging from heart arrythmia (long QT-syndrome) and deafness to epilepsy and ataxia (see Table 2). Typically, many Kv-channel related channelopathies are correlated with a mutant phenotype that is episodic in nature and appears as a dominant hereditary trait. [Pg.1312]

Wernicke s syndrome is a serious consequence of alcoholism and thiamine (vitamin Bx) deficiency. Certain characteristic signs of this disease, notably ophtalmoplegia, nystagmus, and ataxia, respond rapidly to the administration of thiamine but to no other-vitamin. Wernicke s syndrome may be accompanied by an acute global confusional state that may also respond to thiamine. Left untreated, Wernicke s syndrome frequently leads to a chronic disorder in which learning and memory are strongly impaired. This so-called Korsakoff s psychosis is characterized by confabulation, and is less likely to be reversible once established. [Pg.1315]

Somnolence, agitation, confusion, ataxia, vertigo, CNS depression, nightmares, nausea, constipation, bradycardia, hypotension, respiratory depression Same as amobarbital sodium... [Pg.238]

CNS—somnolence, agitation, confusion, CNS depression, ataxia, nightmares, lethargy, residual... [Pg.240]

The older adult is at greater risk for oversedation, dizziness confusion, or ataxia (unsteady gait) when taking a sedative or hypnotic. The nurse checks elderly and debilitated patients for marked excitement, CNSdepression, and confusion. If excitement or confusion occurs the nurse observesthe patient at frequent intervals (as often as every 5-10 minutes may be necessary) for the duration of this occurrence and institutes safety measuresto prevent injury. If oversedation, extreme dizziness or ataxia occurs the nurse notifies the primary health care provider. [Pg.243]


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Ataxia Atherosclerosis

Ataxia Bismuth

Ataxia Blood plasma

Ataxia Bones

Ataxia cannabis

Ataxia clonazepam

Ataxia episodic

Ataxia fluorouracil

Ataxia intermittent

Ataxia lithium treatment

Ataxia lorazepam

Ataxia manganese

Ataxia oxcarbazepine

Ataxia telangiectasia

Ataxia telangiectasia mutated gene

Ataxia telangiectasia mutated proteins

Ataxia telangiectasia-like disease

Ataxia telangiectasia-mutated

Ataxia telangiectasia-mutated kinase

Ataxia with isolated vitamin E deficiency

Ataxia with vitamin E deficiency

Ataxia with vitamin E deficiency AVED)

Ataxia-telangiectasia and RAD3-related

Ataxia-telangiectasia-mutated protein kinase

Cerebellar ataxia

Enzootic ataxia

Episodic Ataxia/Myokymia

Episodic ataxia type

Freidreich s ataxia

Friedreich ataxia

Friedreichs Ataxia

Friedreich’s ataxia

Friedrichs Ataxia

Friedrich’s ataxia

Gait ataxia

In Friedreich’s ataxia

In ataxia-telangiectasia

Neurogenic muscle weakness, ataxia, and

Neurogenic muscle weakness, ataxia, and retinitis pigmentosa

Persisting ataxia

Sensory ataxia

Spastic ataxia

Spinocerebellar ataxia

Spinocerebellar ataxia type

Topiramate ataxia

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