[Body mass index and serum lipid levels in effect on the incidence and course of migraine]. / Czy wskaznik masy ciala i stezenie lipidów w surowicy wplywaia na czestosc wystepwania i przebieg migreny?

Migraine is a well-known condition for many medical specializations. Some authors evaluate the potential impact of the abnormal body mass index (BMI) and abnormal lipid profile on the vulnerability to migraine and its severity. Regarding the fact that these factors have the inseparable connection with the risk of cardiovascular diseases, some papers bring the hypotheses of the probable role of migraine in the progression of such conditions. Some research suggests a link between abnormal BMI and a risk of migraine and its more severe course. When it comes to a lipid panel in migraine, the most frequent abnormalities are elevated levels of total cholesterol and low-density lipoprotein cholesterol which may contribute to the increased risk of migraine. High-density lipoprotein and triglycerides levels were not contributory in most of the papers. We present the latest views on the mentioned problems focusing on differences in results of the particular works.

A single-fibre EMG study of neuromuscular transmission in migraine patients.

It is known that mutations of CACNA1A, which encodes a neuronal P/Q Ca(2+) channel, are present in patients with familial hemiplegic migraine, and possibly in other types of migraine as well. This calcium channel is also involved in neuromuscular transmission. To assess if the single-fibre EMG (SFEMG) method can demonstrate a neuromuscular transmission deficit in migraine, a group of 26 patients with different types of migraine and 20 healthy control subjects were studied. The migraine patients were divided into three groups: 8 patients with migraine without aura (MoA), 12 with migraine with aura excluding visual aura (MA) and 6 with visual aura (VA). A SFEMG of the voluntarily activated extensor digitorum communis muscle was performed. The SFEMG results were normal in the healthy controls and the MoA group (migraine without aura). Slight neuromuscular transmission disturbances were present in 6/12 (50%) of patients with MA and in 1/6 (17%) of patients with VA. We suggest that abnormal neuromuscular transmission detectable by SFEMG may reflect a genetically determined dysfunction of the P/Q Ca(2+) channels in a subgroup of migraineurs with aura.

[Kennedy's disease: expansion of the CAG trinucleotide]. / Choroba Kennedy'ego: ekspansja trójki nukleotydowej CAG.

Kennedy's disease is a rare X-linked spinal and bulbar muscular atrophy (SBMA). A degenerative process of the motor neurons is associated with an increase in the number of CAG repeats encoding a polyglutamine stretch within the androgen receptor. Despite a distinctive clinical phenotype, SBMA can be misdiagnosed, usually due to the lack of clear family history. Accurate diagnosis is important for genetic counseling and because alternative diagnosis of amyotrophic lateral sclerosis usually means much worse prognosis. We report 2 unrelated patients with Kennedy's disease in whom the clinical diagnosis was confirmed by showing the CAG repeat expansion.

Cytotoxic activity of serum and cerebrospinal fluid of amyotrophic lateral sclerosis (ALS) patients against acetylcholinesterase.

The activity of acetylcholinesterase (AChE) was tested in serum of 20 cases of amyotrophic lateral sclerosis (ALS), 4 "disease controls" and 20 age-matched healthy normals. The AChE activity has been tested also in cerebrospinal fluid (CSF) of 20 ALS patients, 2 "disease controls" and 10 normal subjects. An increase in serum AChE was present in the majority of ALS patients with a mild course of the disease, in the severe ALS group elevated serum AChE activity was a rare finding. Serum ACHE was also increased in multifocal motor neuropathy (MMN). In the majority of mild and severe ALS the CSF AChE activity was decreased. No AChE changes were found in CSF of the "disease controls". Serum and CSF ultrafiltrates of ALS patients and "disease controls" were modifying in vitro the spinal cord AChE activity. In the mild ALS group serum and CSF ultrafiltrates with high molecular weight compounds were decreasing the AChE activity. On the other hand in the severe ALS group serum and CSF ultrafiltrates with low molecular weight compounds were increasing the AChE activity. AChE was modified also in some of the "disease controls", especially in MMN and Guillain-Barré syndrome (GBS) by serum ultrafiltrates containing high molecular weight compounds. The AChE activity in serum and CSF is the consequence of the enzyme leakage from brain, degenerating cholinergic neurons and neuromuscular junctions. We suggest that because of the evoked peripherally divergent changes of the enzyme activity, the AChE values in serum and CSF in ALS do not equal to the degree of the changes in the affected tissues and cannot be taken into account in the prognosis of the disease in particular ALS cases.

Electroencephalography of demented and non-demented Parkinson's disease patients.

We investigated the correlation between electroencephalography (EEG) abnormalities and dementia in Parkinson's disease. Three groups of subjects were examined: Parkinson's disease patients without dementia, Parkinson's disease patients with dementia, and healthy age-matched controls. Dementia was assessed with the use of Mini-Mental State Examination. All subjects underwent a routine EEG examination with determination of arousal reaction to eye opening, hyperventilation and photic stimulation. Demented patients with Parkinson's disease more often showed no response to eye opening and presented more slow wave activity in comparison to non-demented patients and healthy controls.