Clinical Neuroscience



NOVEMBER 30, 2006

Clinical Neuroscience - 2006;59(11-12)

[Objective - To investigate the pathomechanism of essential (ET) and parkinsonian tremor (PT) by studying the correlation between tremor severity and movement-related beta rhythm changes of the human electroencephalogram. Patients and methods - We recorded the electroencephalogram of 10 patients with essential tremor, 10 with Parkinsonian tremor and 10 controls. In a preliminary session we determined the side with lower and higher tremor intensity (T+, T++ respectively), using accelerometry. Subjects pressed an on-off switch in a self-paced manner with left and right thumb. After digitalization of the EEG from Cz, C3, C4 electrodes, the movement reactive beta frequency (MRBF), its minimum/maximum peak power values and their latencies triggered to movement offset were determined. Results - The time course and amplitude of movement related beta desynchronization (ERD) were similar in each group regardless of tremor intensity. In ET tremor severity did not influence post-movement beta synchronization (PMBS) amplitude (PMBSET+=100.98±48.874%, PMBSET++=135.1±92.87%; p=0.231), however it was significantly delayed after the movement of the more tremulous hand (latPMBSET+=1.26±0.566 s, latPMBSET++= 1.57±0.565 s, p=0.003). In the PT group on the side of pronounced tremor the amplitude of PMBS decreased but it was not delayed, compared to the less affected hand (PMBSPT+=115.19±72.131%, PMBSPT++= 77.84±53.101%, p=0.0028; latPMBSPT+=1.4±0.74 s, latPMBSPT++=1.25±0.797 s, p=0.191). In controls the power and latency of PMBS was similar on both sides. Conclusions - The results suggest that neuronal mechanisms underlying PMBS generation are differently affected by ET and PT. Investigation of PMBS might be used for the differential diagnosis of essential tremor and Parkinson's disease.]



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Clinical Neuroscience


FEKETE Tamás Fülöp, VERES Róbert, NYÁRY István

[Herniation of the meninges through a defect of the spinal canal is a spinal meningocele, and is usually located dorsally in the lumbosacral region. Meningoceles are usually part of a complex developmental disorder, or of a systemic disease, or it can be iatrogenic, as well. We report a very rare case of a true anterior thoracic meningocele.]

Clinical Neuroscience



Clinical Neuroscience


VARGA Hedvig, PÁRDUTZ Árpád, TAJTI János, VÉCSEI László, JEAN Schoenen

[Migraine is one of the most common neurological disorder affecting up to 14% of the population. The disease shows sexual dimorphism, thus gonadal steroids may play an important role in its patophysiology. One model of migraine headache is the systemic administration of nitric oxide (NO) donor nitroglycerin (NTG), which triggers a delayed attack without aura in many migraine patients but not in healthy volunteers. NTG is also able to activate the neurons of the caudal trigeminal nucleus in the rat. In our review we summarise the effect of NTG on the expression of some molecules, in the superficial laminae of the spinal portion of trigeminal nucleus caudalis, which play an important role in the pathomechanism of headaches, and the modulatory effect of chronic estradiol treatment. Our data show that NTG was able to modify all the examined substances in the caudal trigeminal nucleus, while chronic estradiol treatment abolished this effect. These data may help to understand the mechanisms by which estrogens influence trigeminal nociception and how nitric oxide triggers migraine attacks.]

Clinical Neuroscience


GÁRDIÁN Gabriella

[Huntington’s disease is an autosomal dominantly inherited progressive neurodegenerative disorder. The main symptoms are choreiform, involuntary movements, personality changes and dementia. Huntington’s disease is a member of a group of diseases caused by CAG repeat expansions. One research aim is to determine the earliest molecular changes associated with Huntington’s disease. There is no possibility for this in humans, but various early changes have been identified in an animal model of Huntington’s disease. They are constructed by excitotoxin causing striatal lesion, or mitochondrial toxins inducing energy impairment, or by generating transgenic mice.]

Clinical Neuroscience



[symptoms. In two thirds of the cases the cause is unknown, this is called “idiopathic peripheral facial palsy or Bell’s palsy”, but several different diseases have to be considered in the differential diagnosis. In this paper we reviewed the case histories of 110 patients treated for “peripheral facial palsy” in the Department of Neurology, Semmelweis University, Budapest in a five year period, 2000-2004. We studied the age, gender distribution, seasonal occurance, comorbidities, sidedness, symptoms, circumstances of referral to the hospital, the initial diagnoses and therapeutic options. We also discuss the probable causes and consequences of diagnostic failures. Results: the proportion of males and females was equal. There was no considerable difference between sexes regarding agedistribution. Of the 110 patients 106 was diagnosed with idiopathic Bell’s palsy, three cases with otic herpes zoster and one patient with Lyme disease. In our material, peripheral facial palsy was significantly more frequent in the cold period of late autumn, winter, and early spring. Diabetes mellitus and hypertension were more frequent than in the general population. 74% of the patients were admitted within two days from the onset of the symptoms. In 37% preliminary diagnosis was unavailable. In 15% cerebrovascular insult was the first, incorrect diagnosis, the correct diagnosis of “Bell’s palsy” was provided only in 16%. The probable causes of diagnostic failures may be the misleading symptoms and accompanying conditions. We examined the different therapies applied and reviewed the literature in this topic. We conclude that intravenous corticosteroid treatment in the early stage of the disease is the therapy of choice.]

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Clinical Neuroscience

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Clinical Neuroscience

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Clinical Neuroscience

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