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Introduction: Restless legs syndrome (RLS) is a movement disorder characterized by an uncontrollable urge to move the legs in response to an unpleasant sensation. The coexistence of RLS and other sleep and mood disorders may require adjustment in the therapeutic strategy. The objective of this study was to determine the prevalence of RLS in adults studied with polysomnography and to evaluate its association with other sleep and mood disorders., Patients and Methods: Descriptive cross-sectional study. We included adults studied with polysomnography between 2015 and 2021. We collected information on their medical history, polysomnographic data and mood and sleep disorders using a self-administered written questionnaire which is part of the routine evaluation of all patients referred to this sleep unit. These variables were compared between patients with and without RLS., Results: We included 406 patients. The prevalence of RLS was 36.7% (n = 149). The presence of fatigue (45.3%), moderate to severe insomnia (38.9%) and depression (45.6%) was higher in subjects with RLS. We did not find differences regarding daytime sleepiness and anxiety symptoms. Periodic Limb Movements (PLM) was not associated with RLS (p = 0.26) and its prevalence was low., Conclusion: The prevalence of RLS in subjects studied with Polysomnography is high and it was associated with clinically significant fatigue, insomnia and depression. These symptoms should be identified in order to establish an adequate therapeutic strategy. The prevalence of periodic limb movements was low and was not linked with RLS. These findings contrast with previous publications. Therefore, it requires additional studies to clarify the cause of this variation.

Fibrocartilagenous embolism (FCE) of the intervertebral disc represents a very rare cause of spinal infarct. Up to now only 33 others cases in human beings have been reported in the literature, most of them diagnosed post mortem. We present a 14-year-old boy who developed acute dorsal back pain after lifting a heavy gate, followed by progressive paraparesis. An MRI of the spine showed a degenerative disc at D10-D11 without compromise of the spinal canal lumen associated with an acute Schmorl's nodule situated in the superior endplate of D11. A week later, a second MRI disclosed an intraxial spinal cord lesion at D7-D8 vertebral level involving the vascular territory of the anterior spinal artery. It also showed an abnormal signal located in the posterior third of the D8 vertebral body. These clinical and neuro-radiological findings are similar to those mentioned in the literature and support the diagnosis of an anterior spinal infarct secondary to a probable fibrocartilaginous embolism. This case highlights the importance of considering this etiology among the causes of spinal cord infarct, especially in young people, and underlines the utility of MRI in its diagnosis in vivo.

Spinal cord cavitation is a frequent finding in optic neuromyelitis (Devic's syndrome) (DS) but it is also, although rarely, observed in patients with multiple sclerosis (MS). The objective of our study was to compare the MRI characteristics of the syringomyelic cavities in 6 patients with DS and 3 patients with MS. All the patients with DS had a relapsing clinical form with normal brain MRI. Spinal MRI revealed unenhanced central cavities which extended more than 3 vertebral bodies and remained unchanged in follow-up studies. Two patients presented multiple cavities.MS patients suffered a relapsing remitting form of the disease, they all had hyperintense T2 enhancing lesions on their spinal MRI. Moreover spinal MRI also revealed non communicating cavities which extended less than 2 vertebral bodies. Follow-up studies in MS patients revealed a reduction of both the spinal lesions and the cavities. It is still debated whether DS represents a distinct clinical entity different from MS. These findings help distinguishing both disorders in cases when spinal cavities are present and also contribute to the therapeutic choice.

CADASIL disease (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) was described in 1991 by Tourmier-Lasserve. Two years later the same authors described its association with chromosome 19; nonetheless, the mutations in gene Notch3 were not described until 1996. Clinical findings depend on the age at onset. The early form of the illness is found in young patients, generally less than 30 years old, and the main clinical manifestation is a migraine headache with subcortical lesions in the white matter, while in the later form ischemic events and behavioral symptoms are predominant. Anatomo-pathological findings in CADASIL include the presence of osmophilic granular deposits in vessel walls, skin, muscles and cerebral arteries. We present a patient with CADASIL and cavernous angioma. We studied a 40-year-old woman who underwent surgery for a left temporal-parietal cavernous angioma, with aphasia as the only symptom, two years before admission. Her family history showed that her father had suffered from vascular dementia. She was admitted to our hospital with right-side hemiparesis and dysarthria. A CT scan showed the presence of ischemic vascular lesions and former surgery sequelae. The duplex scan of the neck vessels and a transesophageal echocardiogram ruled out an embolic source. Laboratory tests including VDRL, HIV, prothrombotic profile and rheumatologic screening tests were normal. An MRI in T2W and FLAIR showed the presence of multiple subcortical cerebral lesions and hyperintensity in the white matter (leukoencephalopaty). We found a left acute putaminal-capsular infarct in the diffusion-MRI. The MRA was normal. Analysis of the cerebrospinal fluid was unremarkable. A molecular DNA test was performed, and a nucleotide substitution in position 583 in exon 4 of gene Notch3 was detected. This mutation was found only in CADASIL patients. The association with cavernous angioma has not been previously reported, and we believe that it was unrelated to CADASIL, either clinically or genetically. To our knowledge, this is the first case of CADASIL diagnosed by molecular DNA test in our country.

Intracranial pressure (ICP) monitoring has been shown to improve clinical-pharmacological treatment of intracranial hypertension (ICH) in a rising number of situations, assuring effective cerebral perfusion pressure (CPP) and, concomitantly, reducing the risk of brain ischemia. Although its use in entities such as eclampsia have been reported, the continuous use of ICP monitoring is restricted. We report the case of an eclampsic woman in whom ICP was monitored. Recordings allowed CPP to be correctly stabilized, with strict correlation between ICP and tomographic measurements of density. We also review the pathophysiologic mechanisms that have been proposed to cause ICH in eclampsia and emphasize the usefulness of ICP monitoring to manage this complication.

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.

Prolongation of the QT interval, either on a congenital or an acquired basis, is associated with an increased likelihood of malignant ventricular arrhythmias with a high rate of morbimortality. Symptoms are variables, and patients may develop seizures, syncope and sudden death. Herein we report a young woman 17 years old with long QT syndrome, seizures and recurrent attacks of syncope; her initial diagnosis was primary epilepsy. An electrocardiogram performed 3 years after the initials symptoms was able to make the diagnosis long QT syndrome. The specific treatment controlled the malignant ventricular arrhythmias and the symptomatic status of this patient.

The common signs of hypoglycemia include: tachycardia, diaphoresis and vertigo which may be associated to disturbances of the consciousness. Occasionally, focal neurological signs occur with conservation of consciousness which are erroneously interpreted as cerebral vascular disease. An insulin dependent diabetic patient is presented with an initial diagnosis of transient ischemic attack (TIA) with right hemiparesis and dysarthria associated to hypoglycemia (35 mg %) whose remission occurred following the correction of glycemia. The different physiopathogenic mechanisms were also revised postulating (selective neuronal vulnerability, vasospasms and subjacent vascular disease) and the need for considering this diagnosis must be emphasized in those diabetic patients with focal neurological symptoms.

As Parkinson's disease worsens, many patients develop motor fluctuations which usually correlate directly or indirectly with L-dopa plasma levels. A new L-dopa-benserazide HBS preparation (Madopar) a control release pharmaceutical formulation which is activated when it contacts gastric fluid thus providing more stable L-dopa plasma levels, was assayed. Ten patients with a diagnosis of idiopathic Parkinson's disease and motor fluctuations otherwise unresponsive to conventional therapy were selected. The average age was 62 years and the duration of the disease 9 years. The motor status was evaluated on an hourly basis with the King's College Parkinson's disease rating scale; in addition, a nocturnal disability scale (Lees) was used. Out of the 10 patients, 2 dropped out within the first month due to worsening of parkinsonian signs, while 7 of the remainders preferred HBS preparation to the previous treatment. The number of off hours in this group was reduced by 58% and motor fluctuation became less severe. In only 3 cases was it possible to use HBS as monotherapy while in the rest standard L-dopa had to be added, specially as morning doses. The average L-dopa daily dose was increased by 36%. Unwanted effects included psychiatric disturbances in two (in one L-dopa dose had to be reduced) and epigastralgia in one. Our findings suggest that this L-dopa-benserazide control release may be considered an able therapeutic formulation in the control of motor fluctuations in Parkinson's disease.

We describe a patient with a longstanding paraplegia who developed spinal myoclonus on 3 different occasions spanning one year, once after an enhanced CT scan and twice after excretory urographies, one of which was also followed by a generalized tonic-clonic seizure. To our knowledge only one case of spinal myoclonus secondary to the administration of intravenous contrast material in a patient with a spinal arteriovenous malformation has yet been reported. Taken together, the findings in these cases suggest that spinal myoclonus following intravenous iodine administration is indicative of an underlying spinal cord lesion.