RESUMO
We present the case of a 72-year-old woman with a history of a bipolar mood disorder chronically treated with lithium. Upon having the dose increased, she developed an acute confusional state accompanied by blepharospasm (BS) and apraxia of eyelid opening. Gait instability with frequent falls, pyramid tract signs, and postural tremor in both hands were also evident. On withdrawing lithium, symptoms remitted within 2 weeks. This patient illustrates that BS and apraxia of eyelid opening may be triggered by lithium overdose. Our case warrants the inclusion of lithium in the list of drugs liable to induce such movement disorders.
Assuntos
Antimaníacos/intoxicação , Apraxias/induzido quimicamente , Blefarospasmo/induzido quimicamente , Cloreto de Lítio/intoxicação , Idoso , Antimaníacos/sangue , Transtorno Bipolar/sangue , Transtorno Bipolar/tratamento farmacológico , Pálpebras/efeitos dos fármacos , Pálpebras/fisiopatologia , Feminino , Humanos , Cloreto de Lítio/sangueRESUMO
A previously healthy 10-year-old girl developed a right hemiparesis with sensory loss secondary to a posterolateral thalamic infarct. Despite improvement in strength, three weeks later a 4 Hz kinetic tremor appeared in the right hand accompanied by dystonia in the right upper and lower limbs. Basal ganglia vascular lesions are rare in childhood and movement disorders secondary to such lesions even more so. A thorough work-up failed to disclose the etiology. Our patient illustrates that dystonia and tremor secondary to posterolateral thalamic infarctions are also apt to occur in children and, unlike the adult picture, abnormal movements may develop very soon after the insult.
RESUMO
Two brothers developed hemifacial spasm at 63 and 70 years of age. Spasms occurred on the left and right sides of the face, respectively. Computed tomography scan and magnetic resonance imaging failed to show any abnormality. In addition, a third sibling reported a history of a peripheral facial palsy, which remitted spontaneously without sequelae. This is the fourth description of familial hemifacial spasms. This family is unique in that hemifacial spasm presented on different sides in the two brothers, and involvement was limited to one generation. Age at onset was later than for other familial cases and similar to sporadic cases.
Assuntos
Músculos Faciais/inervação , Doenças do Nervo Facial/genética , Lateralidade Funcional/genética , Transtornos dos Movimentos/genética , Espasmo/genética , Idoso , Doenças do Nervo Facial/fisiopatologia , Lateralidade Funcional/fisiologia , Humanos , Masculino , Transtornos dos Movimentos/fisiopatologia , Contração Muscular/genética , Contração Muscular/fisiologia , Exame Neurológico , Linhagem , Espasmo/fisiopatologiaRESUMO
Argentina is facing an increase in cocaine use by adolescents and young adults from every socioeconomic background. It is calculated that up to 10% of all cocaine passing through this country is locally sold and consumed. Nevertheless, local information describing common cocaine-related neurological events is scarce. From August 1988 to March 1993, 13 patients were evaluated with neurological disease associated with cocaine abuse. Among these 13 patients (Table 1), the mean age was 29; 70% were men. Patients most commonly used the nasal route (snorting). Concomitant abuse of other intoxicants, especially alcohol, was frequent (85%). The major neurological complications included one or more seizures (n = 7), ischemic stroke (n = 2) (Fig. 1-2), hemorrhagic stroke (n = 2) associated with arteriovenous malformation (Fig. 3a-b), memory disturbances (n = 1) and paroxysmal dystonia (n = 1). Psychiatric complaints were present in all patients. Mortality was not observed. There was no correlation between the appearance of complications and the amount of cocaine used, or prior experience with this drug. Only one of the 7 patients with seizures had a previous history of seizures. All had generalized tonic-clonic seizures, and one had concomitant absence episodes. Cocaine modulates central neurotransmitters and has direct cerebrovascular effects. The neurological complications appear to be related to cocaine hyperadrenergic effects, striatal dopaminergic receptor hypersensitivity and perhaps vasculitis. Structural changes in the brain of long-term cocaine abusers could explain the persistence of neurologic symptoms after drug withdrawl.
Assuntos
Encefalopatias/etiologia , Cocaína , Transtornos Relacionados ao Uso de Substâncias/complicações , Adolescente , Adulto , Alcoolismo/complicações , Coma/etiologia , Distonia/etiologia , Feminino , Humanos , Masculino , Parestesia/etiologia , Convulsões/etiologia , Tomografia Computadorizada por Raios XRESUMO
Argentina is facing an increase in cocaine use by adolescents and young adults from every socioeconomic background. It is calculated that up to 10
of all cocaine passing through this country is locally sold and consumed. Nevertheless, local information describing common cocaine-related neurological events is scarce. From August 1988 to March 1993, 13 patients were evaluated with neurological disease associated with cocaine abuse. Among these 13 patients (Table 1), the mean age was 29; 70
were men. Patients most commonly used the nasal route (snorting). Concomitant abuse of other intoxicants, especially alcohol, was frequent (85
). The major neurological complications included one or more seizures (n = 7), ischemic stroke (n = 2) (Fig. 1-2), hemorrhagic stroke (n = 2) associated with arteriovenous malformation (Fig. 3a-b), memory disturbances (n = 1) and paroxysmal dystonia (n = 1). Psychiatric complaints were present in all patients. Mortality was not observed. There was no correlation between the appearance of complications and the amount of cocaine used, or prior experience with this drug. Only one of the 7 patients with seizures had a previous history of seizures. All had generalized tonic-clonic seizures, and one had concomitant absence episodes. Cocaine modulates central neurotransmitters and has direct cerebrovascular effects. The neurological complications appear to be related to cocaine hyperadrenergic effects, striatal dopaminergic receptor hypersensitivity and perhaps vasculitis. Structural changes in the brain of long-term cocaine abusers could explain the persistence of neurologic symptoms after drug withdrawl.