Blepharospasm and apraxia of eyelid opening in lithium intoxication.

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.

Dystonia and tremor secondary to a pediatric thalamic stroke.

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.

Familial hemifacial spasm.

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.

[Neurologic complications by cocaine abuse]. / Complicaciones neurológicas por abuso de cocáina.

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.

Complicaciones neurológicas por abuso de cocáina. / [Neurologic complications by cocaine abuse]

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.

Effect of bromocriptine on neurophysin secretion in pregnant women in labour.

In order to determine whether dopamine plays a role in the control of neuropituitary function in pregnant women during labour, blood levels of nicotine (NSN)- and estrogen (ESN)-stimulated neurophysins were measured in 119 women treated orally with placebo (n = 59, control group) or 5 mg bromocriptine, a potent dopaminergic receptor agonist (n = 60, experimental group). Serum samples were taken before drug ingestion (basal sample) and at delivery. The serum basal concentrations of NSN and ESN were similar in both groups of pregnant women in labour. At delivery, serum ESN levels were similar in all women regardless of the treatment, whereas NSN concentrations were significantly lower in the bromocriptine-treated women than in those who were given placebo. In additional experiments the effect of 5 mg bromocriptine on the serum concentrations of NSN and ESN was tested for 6 hours after drug ingestion in 10 healthy, non-pregnant women and in 8 women in the 3rd trimester of pregnancy. Bromocriptine did not modify the circulating levels of NSN and ESN in either of these 2 groups of women. Since NSN and ESN are thought to be associated with vasopressin and oxytocin, respectively, these results indicate that in non-pregnant women and in pregnant women during late pregnancy dopaminergic stimulation with a dopaminergic receptor agonist does not inhibit the release of either vasopressin or oxytocin during rest. In contrast, dopaminergic receptor stimulation appears to play an inhibitory role in the regulation of vasopressin, but not oxytocin secretion in pregnant women in labour.

Cord blood iodothyronine and thyrotropin concentrations in newborns of mothers exposed to povidone iodine in the last trimester.

In the present study, we have evaluated thyroid function in neonates at delivery and in their mothers who used vaginal povidone-iodine (PVP-I) during the last trimester of pregnancy. Newborns and their mothers without a history of iodine exposure, admitted to the same department and residing in the same geographical area served as controls. Maternal serum thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3) and thyrotropin (TSH) concentrations at delivery were not significantly different between the two groups of pregnant women. Cord blood thyroid hormone concentrations in the newborns of iodine exposed mothers were not significantly different from those in control newborns. In contrast, cord blood TSH concentrations in the neonates of mothers exposed to PVP-I during the last trimester of pregnancy were significantly higher than values in control neonates (p less than 0.05). These data confirm that the fetal thyroid gland, even in the last trimester of pregnancy, does not adapt completely to the inhibitory action of iodine on thyroid hormone synthesis and/or release.