The aim of the paper is to acquaint neurologists, psychiatrists, geriatricians, and other specialists with the options of and practical experience with the laboratory assessment of tau protein, phospho-tau protein, and beta-amyloid in the cerebrospinal fluid in Alzheimer's disease in particular. The rationale for the use of the three cerebrospinal fluid biomarkers is briefly summarized, the principle and the methodology of the cerebrospinal fluid test are explained in detail, including an evaluation of an own group of patients, and requirements for a proper sample collection technique are emphasized. When evaluating the three cerebrospinal fluid AD biomarkers in Alzheimer's disease, the sensitivity and specificity increase to 85–94 % and 83–100 %, respectively. Thus, patients with minimal cognitive deficit who are at a higher risk of developing Alzheimer's disease can be expected to benefit greatly from an evaluation of AD biomarkers.

Professional and Non-professional Intoxications with Lesion of the Central Nervous System in the Years 2005–2009 Reported by the Czech National Registry of Occupational Diseases and The Czech Toxicological Information Center The authors inform the readers on the number of professional and non-professional intoxications with lesion of central nervous system in the Czech Republic in years 2005–2009 (till 30. 10. 2009). The article is based on data reported by the Czech National Registry of Occupational Diseases, which is administered by the National Institute of Public Health in Prague, and by database of the Czech Toxicological Information Center in Prague. of Occupational Diseases, Czech Toxicological Information Center.

The goal of the general therapy for acute cerebral infarction is to prevent the progression of cerebral ischemia as well as to prevent and treat complications. It is of utmost importance to ensure adequate oxygenation and cerebral perfusion pressure. It is essential to maintain normothermia, to maintain optimum hydration and internal environment conditions, to initiate enteral nutrition early, and to provide prophylaxis against thromboembolic disease. In the acute phase of cerebral infarction, hypertension, tachycardia, and psychomotor agitation are commonly encountered and epileptic seizures may occur. Decompressive craniectomy can be a life-saving procedure in patients with a large cerebral infarction.

Clinical case report Glycogenosis type II (GSD II) is a lysosomal storage disorder caused by insufficient activity of acid α-glucosidase (acid maltase). This enzyme is responsible for the degradation of intralysosomal glycogen. Accumulation of glycogen in lysosomes leads to the cellular dysfunction and damage in many organs and tissues. GSD is inherited in autosomal recessive trait, the incidence is panethnic approximately 1 : 60 000 of live-born children, the gene for α-glucosidase is localised on chromosome 17 (17q23). We differentiate the classical infantile onset type with first symptoms within the first few months of life, with generalized muscle weakness and hypotonia (floppy baby), hepatomegaly, progressive cardiomyopathy and death in first two years and the late-onset form presentating anytime during childhood or adulthood with slow progression of muscle weakness of legs, arms, trunk and diaphragm, but without cardiac involvment. In biochemical assessment we find elevation of creatinkinase, AST (SGOT), ALT (SGPT), LDH, the glycide metabolismus is normal, in clinical test with muscle ischemia we observe normal elevation of lactate in venous blood. Electromyography is with typical pseudomyotonic changes but with normal nerve conduction velocity. In muscle biopsy we see increased amount of structural normal glycogen in lysosomes and also intracellular. Diagnosis of Pompe disease is confirmed by low or absent acid α-glucosidase activity in cultured skin fibroblasts, purified lymphocytes, leucocytes or muscle cells. In last year we can also use a non-invasive acarbose-based assay performed on dried blood-spots. Mutation analysis can help in final verification of Pompe diagnosis. Prenatal diagnosis is possible due to DNA analysis or enzymologic assay in amniocytes or chorion villi samples. The only effectual treatment is the enzyme replacement therapy (ERT). Myozyme (alglucosidase alfa) is purified recombinant enzyme administered beweekly in short intravenous infusion in recommended dosis 20 mg/kg. Other treatment options, used in lysosomals storage disorders, like haemopoetic stem cell transplantation, substrat inhibition therapy, chaperons or gene therapy, are not suitable for GSD II. Palliative care and symptomatic therapy like ventilation support and physical therapy can be effective in managing symptoms, but can not prevent the disease progression. The diet with low sugar for glycogenolysis stimulation and high protein intake are of questionable effect. In the case report we present our experience with ERT in 37-year old patient with confirmed GSD II diagnosis.

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 and practiced. We briefly summarize the current state of knowledge and practical approach to the management of intracranial hypertension using the above substances and we also point to certain widely accepted fictions that probably lack any rational background.

Bladder atonia and areflexia are functional consequences of spinal shock following SCI. Sphincters are inactive, voiding is not possible. The bladder is distended. During this acute phase the therapeutic aim occurs in ensuring of the urine derivation preventing complications. Following procedures are used: permanent indwelling catheter, suprapubic drainage, intermittent cathe terization, reflex voiding by bladder tapping and suprapubic manual pressure. First days after injury on the ICU, a permanent indwelling catheter is used, later on changed to suprapubic drainage. It is recommended to change to intermittent catheterization as early as possible. Related to the level of injury the catheterization by themselves is trained for. Presence of urine infection can influence these algorithms. An adequate therapy of urine infection prevents bladder stone formation. Basic diagnostic for detrusor-sphincter dyssynergy during the chronically phase is the video-urodynamical assessment. Therapy is difficult, it occurs in a sufficient derivation. Pharmacological therapy mainly is focused to reduce the hydrostatic pressure in the urine system. Beside suprapubic epicystostomy surgical procedures are described. Those procedures support continence or provide for permanent incontinence (urinal).

Epileptic as well as non-epileptic seizures are frequent problem in teenage. Both intrinsic (e. g. estrogens/gestagens rate) and exogenic (e. g. sleep deprivation and first experiences with alcohol). Psychosocial and neurovegetative instability should be causative factor of high incidence of non-epileptic or migrenous attacks.

The complexity of the topographic relations of the spine, spinal cord, and spinal nerves is a result of the incongruous growth of the spine and the spinal cord, the growth of which is retarded from the third month of embryonic development. The spinal cord only extends to the upper portion of the lumbar spine and the spinal nerves run obliquely down the spinal canal. Those spinal cord segments that were originally situated at the level of the corresponding vertebrae are located above the vertebral bodies. From the level of the second lumbar vertebra down the spinal canal, only spinal roots are found resembling a horse's tail (cauda equina) in appearance. In contrast to the intracranium, the morphology of the epidural space and of venous drainage is different.

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 logical diagnostic process and principles of therapy should contribute to further proceedings in care of these patients.

Choreatic dyskinesias are caused by the hetegenous dysfunctions of basal ganglia system. For clinical settings we have several options: antipsychotics (i. e. risperidone, tiapride), presynaptic dopamine depletors (tetrabenazine), GABAergics (clonazepam), antiglutamatergics (i. e. amantadine). Their intensity could be pharmacologically controlled, at least partially, however their causal curability is only seldom available.