Neurol. praxi. 2009;10(1):3
Neurol. praxi. 2009;10(1):8
Neurol. praxi. 2009;10(1):9-12
The article shortly summarizes the associations of intracranial hypertension and its symptoms in the light of its pathophysiological bases. The main symptoms of intracranial hypertension are listed as well as the clinical descriptions mentioned in the past by reputable Czech neurologists.
Neurol. praxi. 2009;10(1):13-18
Intracranial hypertension has a number of causes with converging mechanisms of secondary brain damage. Vascular autoregulation, blood-brain barrier disruption, membrane depolarization, biochemical cascade with glutamate and free radicals´ effects, and mechanisms of interstitial and intracellular edema are analysed. Common and specific therapeutic measures based on these pathophysiological processes are derived: complex monitoring including intracranial pressure, cerebral perfusion pressure control, sedation, analgesia, therapeutic hyperventilation, barbiturate coma, external ventricular drainage, decompressive craniectomy with focus on new indications in...
Neurol. praxi. 2009;10(1):19-23
Every neurologist is familiar with usage of osmotically active substances and glucocorticoids in the treatment of intracranial hypertension – these medicaments were introduced into clinical practice more than 50 years ago and the abundant literature supporting their role in this indication is convincing. Bearing this in mind, it is even more interesting that we still don’t know the precise mechanism of their action and there is no consensus regarding the ideal dosage of osmotically active substances, timing of treatment and their effectiveness in different indications. Established treatment algorithms are, however, universally accepted...
Neurol. praxi. 2009;10(1):24-27
Neurosurgical options for the management of intracranial hypertension are based on the concept of primary and secondary brain damage. A primary insult cannot be affected; therefore, neurosurgical as well as other treatment modalities aim at minimizing secondary brain damage. The authors review the neurosurgical treatment modalities of intracranial hypertension dividing them into three groups: 1. evacuation procedures during which the pathologically increased tissue volume is removed; 2. derivation procedures allowing a decrease in intracranial pressure by evacuation of cerebrospinal fluid; 3. decompressive craniectomies enabling a decrease in...
Neurol. praxi. 2009;10(1):28-31
These guidelines have been developed to assist practical neurologists, geriatricians, psychiatrists, and other specialists involved in the care of patients with dementia. The paper is grounded on scientifically based treatment procedures that are mainly based on double-blind, placebo-controlled studies and meta-analyses. We present the guidelines for the treatment of Alzheimer‘s disease, vascular dementia, Parkinson‘s disease with dementia, and dementia with Lewy bodies. These guidelines should result in rational and effective treatment procedures in the most common types of dementia.
Neurol. praxi. 2009;10(1):32-36
Peripheral neuropathies represent various disturbances of peripheral nervous system and according to localization of peripheral nervous system lesions (neurons, roots, ganglia, nerves), distribution and extend of lesions (mononeuropathies to polyneuropathies), type of lesion (axonal, demyelinisation, mixed), and clinical course (acute, chronic, remitting, steadily progressive) are differing one from another. Patients with peripheral neuropathies are often coming to neurological outpatients’ clinics. A successful diagnosis and a satisfying therapy use to be a difficult problem. An overview of basic aspects of neuropathies with suggestion of...
Neurol. praxi. 2009;10(1):39-43
Abnormal head posture is a frequent but nonspecific symptom in children. In young children, in particular, it may be the first manifestation of a serious condition. The causes may vary significantly and the severity may range from benign to very severe, life-threatening conditions. Aetiology differs from that in adult patients and a number of clinical entities are entirely specific to child age. The paper deals with the differential diagnosis of frequent as well as rare clinical entities occurring in child age in which this may be the presenting symptom; they are divided according to the age at which most commonly manifested.
Neurol. praxi. 2009;10(1):44-48
Pompe disease, or glycogen storage disease type II, is a rare autosomal recessive disorder caused by mutations in the gene that encodes for α-glucosidase. Presentation in infancy is associated with severe muscle weakness, cardiomyopathy and respiratory failure. Juvenileand adult-onset typically present with proximal muscle weakness and are associated with exertional dyspnoe or respiratory insufficiency. Determination of α-glucosidase activity in a dried blood spot provides a rapid and reliable diagnostic method for Pompe disease, especially as the initial screening test. Confirmatory testing should be performed by measuring of α-glucosidase...
Neurol. praxi. 2009;10(1):54-57
Antiphospholipid syndrome (APS, also called as Hughes syndrome) is a relatively common autoimmune disorder characterized by recurrent arterial or venous thromboses and/or pregnancy-related complications with a characteristic finding of antiphospholipid antibodies. To diagnose APS, the following criteria must be met: one clinical criterion (i. e., the presence of thrombosis or repeated abortions or preeclampsia) and one laboratory criterion, i. e., the demonstration of some of the antiphospholipid antibodies within a minimal time interval of 12 weeks between individual laboratory tests. Antiphospholipid antibodies interfere with the homeostasis...
Neurol. praxi. 2009;10(1):50-53
Huntington’s disease is a hereditary neurodegenerative disease primarily affecting striatal neurons, manifested mostly in adulthood by a combination of neurological and psychiatric symptoms, most typically by choreatic hyperkinesias and development of dementia. We report a case of a female patient with Huntington’s disease presenting as multisystem atrophy (MSA) with delayed manifestation of chorea. Unlike a typical MSA presentation, asymmetry in manifestations of Parkinson’s syndrome and responsiveness to levodopa were evident.
Neurol. praxi. 2009;10(1):58
Neurol. praxi. 2009;10(1):60-62