Leg cramps in relation to metabolic syndrome.

A leg cramp is a pain that comes from a leg muscle. It is due to a muscle spasm which usually occurs in a calf muscle, below and behind a knee. Leg cramps (often called night cramps) usually occur most commonly at night when in bed. Night leg cramps are involuntary painful contractions of skeletal muscles arose in the calves and soles of the feet. Although in most cases they aren't harmful and resolve easily in some instances they have a long duration and can result in intense pain, disturb normal sleep and make a person feel anxious. Pathophysiology of leg cramps is poorly understood. The aim of our study was to determine the role of metabolic syndrome in relation to night leg cramps. The study included 86 subjects aged 34 to 88 years. Metabolic syndrome group consisted of 40 subjects (10 men (25%) and 30 women (75%)); the control group consisted of 46 persons (9 men (19.5%) and 37 women (80.5%)). According to frequency and intensity of manifestation leg cramps were subdivided into less frequent and frequent leg cramps. Blood samples were analysed for lipids, fasting glucose, red blood cells and electrolytes. Persons were screened for leg vein insufficiency as well. The investigation showed that 77.5% (31/40) of patients with metabolic syndrome had leg cramps, from which 60% (24/40) had frequent leg cramps. In control group 73.9% (34/46) had leg cramps, from which 50% (23/46) had frequent leg cramps. Among known predisposing factors leg cramps most often were associated with deep vein insufficiency and superficial vein varicose. High frequency of night leg cramps in our study is due to female predominance (75% versus 25% women and men, respectively) and age distribution in our study population (from 34 to 88 years old). The investigation showed that people often experience nocturnal leg cramps. Leg cramp is slightly increasing among the patients with metabolic syndrome. Frequent leg cramps were observed in 60% of cases in metabolic syndrome group versus 50% of cases in controls.

[Basal ganglia calcification: clinical manifestations and diagnostic evaluation].

Physiological intracranial calcification occurs in about 0,3-1,5% of cases. It is asymptomatic and is detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases and other. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism doesn't respond to drugs containing levodopha. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders (blood calcium level and other), those are: Cockayne syndrome, tuberous sclerosis, Fahr's syndrome, Down syndrome and other. We observed some cases of basal ganglia calcification and studied clinical manifestations and treatment tolerance of this pathological condition. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyreoid hormone is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. Basal ganglia calcification in young patient with acute hepatitis may be result of Wilson disease.