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R Gilad

Publications and source records attributed to R Gilad.

35 records · Page 2Linked to original sources

Early treatment of a single generalized tonic-clonic seizure to prevent recurrence.

BACKGROUND: The question of whether to start antiepileptic treatment after a single unprovoked seizure remains controversial and has been the subject of much debate in the relevant literature. OBJECTIVES: To determine the rate of recurrence of a second attack after a single unprovoked epileptic seizure by using 2 study groups of treated and untreated patients and, thus, to establish a treatment policy for these patients. PATIENTS AND METHODS: A group of 91 patients with a single generalized tonic-clonic seizure were prospectively studied; 87 of these patients completed the study. The end point of the study was 36 months after the single attack or the occurrence of a subsequent epileptic attack. The patients were randomly divided into 2 groups; 45 patients who immediately received anticonvulsive treatment and 42 who remained untreated for the follow-up period. Patients in the treated group were given monotherapy with carbamazepine. The results of recurrences were statistically analyzed by using the Kaplan-Meier method. RESULTS: Results indicated a significantly higher percentage of seizure-free patients in the treated group compared with that in the untreated group (P = .001). The treated men were proved to be less at risk for recurrent seizures compared with treated women (P < .001 vs P = .03, respectively). CONCLUSION: Treatment after a single unprovoked seizure leads to a significant reduction in the risk of relapse of generalized tonic-clonic epilepsy.

Adult↗

Strokes mimicking peripheral nerve lesions.

Sensory-motor deficit in a peripheral nerve pattern due to brain lesion is rarely documented. We report on seven patients with a clinical manifestation of sensory-motor deficit, imitating peripheral nerve involvement, due to lacunar brain infarcts verified by brain computed tomography scan. Five of the patients had an ulnar nerve-like deficit and two median nerve-like deficits. The infarcts were located in the thalamus and the corona radiata. No clinical or electrophysiological evidence for peripheral nerve involvement was found. The unusual peripheral nerve pattern of lesions caused by lacunar brain infarcts can be defined as an additional lacunar syndrome and must be taken into consideration in the clinical evaluation of peripheral nerve deficits with normal nerve conduction velocity.

Aged↗

Peripheral neuropathy in multiple sclerosis: a clinical and electrophysiologic study.

Peripheral nerve abnormalities are uncommon in multiple sclerosis (MS). When present, they are usually attributed to factors associated with advanced disease, such as malnutrition or cytotoxic drugs. We prospectively evaluated 22 mildly disabled MS patients with sensory complaints for evidence of neuropathy using the Neuropathy Symptom Score (NSS), clinical examination, and electrophysiologic studies of peripheral nerves. Distal latency, F-wave response, and nerve conduction velocity (NCV) and amplitude in the ulnar, median, tibial, peroneal and sural nerves were examined. Neuropathy was recorded if electrophysiologic abnormalities were detected in at least two peripheral nerves in the same patient. The most frequent electrophysiologic abnormalities noted were prolonged F-wave response and low motor amplitude in the peroneal nerve, slow sensory conduction velocities of the ulnar and sural nerves, and prolonged distal latencies in the sensory ulnar and sural nerves. Electrophysiologic abnormalities were found in 33 of 244 nerves examined (14.7%) and occurred in 10 patients (45.5%). Neuropathic symptoms were mild and did not correlate with electrophysiologic abnormalities. Age, disease duration, disease course and neurologic disability as evaluated by the Kurtzke Expanded Disability Status Scale, were not associated with the presence of neuropathy. Our findings indicate a high frequency of sensory-motor neuropathy in a selected group of MS patients.

Adolescent↗

Neurological and functional outcome in patients with supratentorial hemorrhages. A prospective study.

BACKGROUND AND PURPOSE: A prospective study was performed to evaluate neurological and functional outcome after spontaneous supratentorial bleeding. The aim of the study was to determine whether clinical or neuroradiological parameters could predict the outcome of these patients during the first hours of hospitalization. METHODS: Two hundred seventy-nine patients--52 with thalamic, 87 with putaminal, and 140 with lobar hemorrhages--were followed prospectively and examined on admission and at 2 weeks, 3 months, and 6 months after onset. The patients underwent clinical (according to the Glasgow Coma Scale) and neuroradiological examinations on admission and were scored clinically and functionally (according to Stroke Severity score and Barthel Index) on the follow-up periods. Risk factors and the correlation between findings on admission and the latest clinical and functional results were calculated with the chi 2 test, Pearson correlation test, and Student's t test. Multivariate analysis was calculated with the stepwise regression test. RESULTS: In all of the bleeding locations, lethal outcome was significantly correlated with size of the hematoma (P < .001) and Glasgow Coma Scale score on admission (P < .001). Intraventricular blood expansion was found to have a better prognosis in thalamic bleeding (P < .007) and a worse prognosis in lobar hemorrhage (P < .01). The functional outcome after 6 months was directly correlated with the size of the bleeding area in lobar and putaminal hemorrhages. No correlation was found in thalamic bleeding. A worse functional outcome was found in putaminocapsular bleeding (P = .004) and in patients with ischemic heart disease. A limited better recovery prognosis was found in patients with lobar hematoma in the temporal lobe (P = .052). CONCLUSIONS: The probability of lethal outcome can be calculated on admission in all patients with supratentorial bleeding and in correlation with the location and size of the bleeding area and level of consciousness. Intraventricular expansion of blood is a better prognostic factor in thalamic bleeding and a worse one in lobar hematoma. Functional outcome is correlated with size of the bleeding area and level of consciousness on admission in putaminal and lobar hemorrhages but has no correlation to thalamic hemorrhage.

Age Factors↗

[Effect of low-dose amiodarone on thyroid function].

Thyroid function was examined periodically in a group of 85 patients treated with low-dose amiodarone, and followed for 1-13 years (mean 3.6). Biochemical hypothyroidism (elevated thyroid stimulating hormone (TSH) only) developed in 8 patients and clinical hypothyroidism in 3, while hypothyroidism developed in 5. In the first 11 cases amiodarone was continued but 1-thyroxine was added. In the 5 that became hyperthyroid, amiodarone was stopped and thyroid function became normal within a few months. In the 69 patients without thyroid dysfunction, elevated thyroxine (T4) and free thyroxine index (FTI) were found in 20% and 17%, respectively, and elevated free T4 (FT4) in 28%; all had normal total tri-iodothyronine (TT3) and TSH. In practically all patients, reverse T3 (rT3) rose more than 30% above initial levels. It is concluded that in patients treated with low dose amiodarone: 1) thyroid function should be followed closely; 2) elevated levels of TT4, FTI and FT4 do not necessarily imply hyperthyroidism; 3) hypothyroidism may be biochemical only, without progression to overt hypothyroidism, despite continued treatment; 4) both the hypo- and the hyperthyroidism induced are usually reversible; 5) amiodarone may be continued despite onset of hypothyroidism, provided replacement therapy is given.

Amiodarone↗

Intravenous gammaglobulin treatment in multiple sclerosis and experimental autoimmune encephalomyelitis: delineation of usage and mode of action.

Multiple sclerosis (MS) is a central nervous system demyelinating disease of implicated autoimmune aetiology. The effect was evaluated of intravenous gammaglobulin (IVIg), a successful therapy in various autoimmune diseases, in relapsing-remitting MS patients treated for three years. IVIg treatment significantly reduced the number and severity of acute exacerbations and resulted in a lesser neurological disability. There were no significant short or long-term adverse effects to IVIg treatment. To clarify the putative therapeutic effects of IVIg, this treatment was examined in the animal model of experimental autoimmune encephalomyelitis (EAE) in the rat. IVIg suppressed active EAE in relation to disease severity and duration, despite the presence of T-cell reactivity to specific antigens, while the treatment had no effect on passive EAE induced by adoptive transfer of myelin basic protein specific CD4 + T-cells. It is concluded that IVIg treatment may be a promising treatment in relapsing-remitting MS as it can alter the natural course of the disease.

Adult↗

Open controlled therapeutic trial of intravenous immune globulin in relapsing-remitting multiple sclerosis.

Ten patients with relapsing-remitting multiple sclerosis were treated with intravenous immune globulin, 0.4 g/kg per day for 5 consecutive days, and then with additional booster doses of immune globulin of 0.4 g/kg, once every 2 months, for the next 12 months. Ten untreated patients with relapsing-remitting multiple sclerosis who were matched with the study patients for age, disease duration, and number of attacks per year served as controls. Immune globulin treatment was well tolerated, with no side effects. The exacerbation rate decreased from 3.7 +/- 1.2 exacerbations per year before treatment to 1.0 +/- 0.7 exacerbations per year during the treatment in the immune globulin-treated patients, while it remained unaltered in the controls. The posttreatment Kurtzke Expanded Disability Status Scale score decreased from a mean of 4.45 to 4.15, whereas in controls it increased from 3.55 to 3.75. The results suggest that immune globulin suppresses the ongoing pathologic process in multiple sclerosis and may be a promising treatment to prevent disease exacerbations.

Adult↗

Giant axonal neuropathy with predominant central nervous system manifestations.

The authors describe a 25-year-old woman with giant axonal neuropathy (GAN) and severe CNS involvement. She had been admitted to hospital with generalized seizures, and had gait disturbances followed by progressive mental deterioration since childhood. Neurological examination revealed mental retardation, scanning speech, cerebellar dysfunction, pyramidal signs, mainly in the lower extremities, and peripheral sensory neuropathy. Sensory nerve conduction velocity was decreased; brain CT and MRI showed diffuse demyelination. Sural nerve biopsy revealed characteristic signs of GAN. The patient's older sister had died at the age of 23, after having had similar neurological disturbances since childhood. This case illustrates an unfamiliar presentation of GAN, characterized by mild sensory neuropathy and serve CNS involvement, including seizures.

Adult↗

[Complications of low-dose amiodarone].

Complications of low-dose amiodarone in 83 patients, in whom the drug was effective and who were followed for 1-13 years, are presented. Hypothyroidism was diagnosed in 11 (in 8 by the finding of elevated TSH). In 2 of the 3 in whom clinical signs of hypothyroidism were evident, amiodarone was continued, but thyroxine was also given. In 5 others thyrotoxicosis ensued. Propylthiouracil (PTU) was given and amiodarone was discontinued. PTU was then stopped within 4-8 months, without recurrence of the hyperthyroidism. In 1 patient pneumonitis resolved spontaneously a few weeks after stopping amiodarone. Because of gastrointestinal distress amiodarone was stopped in 1 patient. In none were liver enzymes elevated, nor was the nervous system affected clinically. Photosensitivity in 6 patients and skin discoloration in 2 did not necessitate discontinuation of the drug. Blurred vision was reported by 4, but its connection with amiodarone was not proven. There was sinus bradycardia in 2. There was no arrhythmic effect of amiodarone seen on ECG nor on Holter monitoring, nor was there any mortality. We conclude that amiodarone in low doses causes many complications, most of them mild and transient. However, in only a few cases is discontinuation of the drug indicated.

Amiodarone↗

Glioblastoma multiforme with bone metastase and cauda equina syndrome.

Remote metastases, leptomeningeal dissemination and spreading of the tumor by infiltration are rare complications of glioblastoma multiforme. The existence of different forms of spreading simultaneously is very rare. We present a case of a young patient with glioblastoma multiforme who was operated and subsequently received radiation therapy and cytotoxic treatment. Eight months following the operation, the patient developed cauda equina syndrome. Bone metastases of vertebrae and ribs, and direct infiltration of the recurrent tumor mass into the ethmoidal and frontal sinuses were found. The described patient demonstrates a very rare combination of all forms of spreading metastases in glioblastoma multiforme. The infiltration of the tumor mass into the sinuses and the direct permeation of the meningeal and dural venous system and of the leptomeninges, may explain the mechanism of the development of distant metastases and leptomeningeal dissemination in glioblastoma multiforme.

Adult↗

Chloral hydrate in intractable status epilepticus.

Five adult patients were admitted to the neurological department in a state of status epilepticus. All were treated unsuccessfully with IV diazepam and diphenylhydantoin. Administration of sodium valporate or phenobarbital also was ineffective. However, after treatment with intrarectal chloral hydrate, all seizures ceased. The excellent effect of this drug was proved both clinically and electrodiagnostically. Discussed is the possibility of using chloral hydrate to treat patients with status epilepticus in whom conventional treatment has failed.

Administration, Rectal↗

Intravenous administration of magnesium sulfate in acute stroke: a randomized double-blind study.

A randomized, placebo-controlled, double-blind study was performed as a pilot study to examine the benefit of the administration of magnesium sulfate given intravenously as a protective substance during the first 24 hours following a stroke. Patients who had cortical infarction in the middle cerebral artery territory with moderate to severe neurologic deficits lasting for more than 15 minutes with onset less than 24 hours were included. The patients were treated with magnesium sulfate or placebo for 5 days and examined by a blinded investigator. Patients had follow-up for 30 days. The primary efficacy variable was the proportion of patients reaching mild to moderate neurologic deficit on the Orgogozo scale (80 points) and relative functional independence on the Barthel index (60 points). Orgogozo scale and Mathew scale values were obtained on admission and days 2, 4, 8, and 30 after stroke. Barthel activities of daily living index and Rankin disability score were obtained on day 30. Forty-one patients (22 given treatment and 19 given placebo) demonstrated significant beneficial effects on the Orgogozo scale (84 +/- 11 vs. 64 +/- 10, p < 0.0001) and (83 +/- 14 vs. 70 +/- 15, p < 0.009), respectively. At the end of 1-month follow-up, the Barthel ADL index was nonsignificantly higher and the Rankin disability score was marginally significantly lower in the magnesium-treated group (84 +/- 26 vs. 71.8 +/- 26, p < 0.143) than in control subjects (2.3 +/- 1.1 vs. 3 +/- 1.3, p < 0.077). Intravenous magnesium sulfate had significant positive effect on the outcome in patients with acute stroke. Further studies on a larger scale are needed to confirm these findings.

Activities of Daily Living↗

Rhabdomyolysis induced by simvastatin and ketoconazole treatment.

Rhabdomyolysis is described as an adverse event of simvastatin therapy either by itself or in combination with other medications. It is unclear whether this phenomenon is specific to simvastatin or to all cholesterol-lowering agents as single-dose therapy or caused by the association of special coadministered medications. We describe two cases in which rhabdomyolysis developed after coadministration of simvastatin (20 mg/d) and the antifungal ketoconazole. The clinical features, blood examination results, and positive outcome were very similar in both cases. We concluded that ketoconazole, an antifungal sterol synthetic inhibitor of the azol group, may induce rhabdomyolysis in patients undergoing treatment with simvastatin, a lipid lowering agent, and increase the possibility of muscle-damaging adverse events of the agents.

Aged↗