Volumetric analysis of cerebrospinal fluid and brain parenchyma in a patient with hydranencephaly and macrocephaly--case report.

The aim of this study was to perform for the first time the intracranial volumetric analysis of cerebrospinal fluid (CSF) and brain parenchyma in the supratentorial and infratentorial space in a 30-year-old female patient with hydranencephaly and macrocephaly. A head scan performed using a 3T magnetic resonance was followed by manual segmentation of the brain parenchyma and CSF on T2 coronal brain sections. The volume of CSF and brain parenchyma was measured separately for the supratentorial and infratentorial space. The total volume of the intracranial space was 3645.5 cm3. In the supratentorial space, the volume of CSF was 3375.2 cm3 and the volume of brain parenchyma was 80.3 cm3. In the infratentorial space, the volume of CSF was 101.3 cm3 and the volume of the brain parenchyma was 88.7 cm3. In the supratentorial space, there was severe malacia of almost all brain parenchyma with no visible remnants of the choroid plexuses. Infratentorial structures of the brainstem and cerebellum were hypoplastic but completely developed. Since our patient had no choroid plexuses in the supratentorial space and no obstruction between dural sinuses and CSF, development of hydrocephalus and macrocephaly cannot be explained by the classic hypothesis of CSF physiology with secretion, unidirectional circulation, and absorption as its basic postulates. However, the origin and turnover of the enormous amount of intracranial CSF volume, at least 10-fold larger than normal, and the mechanisms of macroencephaly development could be elucidated by the new hypothesis of CSF physiology recently published by our research team.

[Selection criteria for parameters of electric current in trans-CSF brain stimulation in patients with posttraumatic vegetative state].

Trans-CSF brain stimulation is on of applied methods of stimulation in posttraumatic vegetative state. The paper analyzes application of this technique under the control by different methods of electrophysiological monitoring. Authors suggest principles of selection of stimulation parameters and detectable criteria of its effectiveness.

[Detection of amino acid neurotransmitters in cerebrospinal fluid of patients in persistent vegetative state].

OBJECTIVE: To detect the amino acid neurotransmitters in cerebrospinal fluid of patients in persistent vegetative state (PVS) to define their relation to the clinical manifestations of the patients. METHODS: The cerebrospinal fluid from 46 patients in PVS and 20 control patients were collected for detection of glutamic acid, aspartic acid, alanine and glycine by high-performance liquid chromatography. RESULTS: All the four amino acids were separated by chromatography within 25 min. The contents of all the 4 neurotransmitters in PVS group were higher than those in the control group, and their contents were inversely correlated to PVS score of the patients. The differences in the concentration of glycine and alanine were significant between PVS patients and the control patients (P<0.05). CONCLUSION: The patient's clinical manifestations are related to the contents of amino acid neurotransmitters in the cerebrospinal fluid of PVS patients.

[The research on monoamine neurotransmitters changes in plasma and cerebrospinal fluid in patients with persistent vegetative state].

AIM: To study the relationships between the pathogenesis of persistent vegetative state (PVS) and the levels of monoamine neurotransmitters in plasmas and cerebrospinal fluids (CSFs) in patients with PVS. METHODS: The high-pressure liquid chromatography (HPLC) was used to detect. RESULTS: It was found that the level of dopamine (1.95 +/- 0.99) was significantly increased in plasma compared with the control (1.16 +/- 0.47) (P < 0.05), but the levels of 5-HT, TYR, TRP, GABA of plasma were insignificantly changed. In cerebrospinal fluid, the level of DA was insignificantly changed, and the level of 5-HT (0.49 +/- 0.32) was significantly decreased compared with the control (1.02 +/- 0.35) (P < 0.05), but the levels of TYR (1.36 +/- 0.11), TRP (0.63 +/- 0.40), GABA (1.15 +/- 0.61) were significantly increased respectively compared with the controls (0.40 +/- 0.24; 0.29 +/- 0.22; 0.37 +/- 0.45) (P < 0.05; P < 0.05; P < 0.01). The levels of GABA and DA in plasma were significant correlated (P < 0.05), and GABA and DA in CSF were also significant correlated (P < 0.01). CONCLUSION: The results of this study suggested that PVS is related to the decrease of 5-HT in CSF and the increase of DA in plasma.

[Monoamines, monoamine metabolites, neuron specific enolase and myelin basic protein concentrations in cerebrospinal fluid of resuscitated patients].

Changes of monoamines, monoamine metabolites, neuron specific enolase (NSE) and myelin basic protein (MBP) levels in cerebrospinal fluid were measured in 8 patients for up to 7 days after cardiopulmonary resuscitation. The outcomes were assessed by the Glasgow Outcome Scale. One showed good recovery 3 developed a persistent vegetate state (PVS) and 4 became brain dead (BD). The concentration of NSE increased to a peak about 3 days after resuscitation, then gradually decreased. MBP also showed an increase with time up to 7 days. The time course suggests that neuronal and/or axonal damage progresses for several days after hypoxic or anoxic brain insult. NSE and MBP in the BD group were higher than those in the PVS group, thus CSF levels may be prognostic with regard to hypoxic brain injury. Tyrosine, dopamine, 3-methoxytyramine (3-MT), 3-dihydroxy-4-phenylacetic acid (DOPAC), homovanillic acid (HVA), vanillylmanderic acid (VMA), normetanephrine (NMN), metanephrine (MN), 3-methoxy-4-hydroxyphenylglycol (MHPG), vanillic acid (VA), tryptophan and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were analyzed by HPLC with an electrochemical detector. Concentrations changed within 2 or 3 days after resuscitation, so concentrations at that period may indicate neuronal damage. However, there are some cases with abnormal NSE and MBP levels without abnormal monoamine levels, suggesting that differences in concentrations are not the consequence of the amount of affected neurons, but of the sites of regions.