Cholinesterase Activity In Cerebrospinal Fluid Research Articles

Cerebrospinal fluid cholinesterase activity in children with meningitis

Cerebrospinal fluid cholinesterase activity in children with meningitis

Safety of Lumbar Puncture Procedures in Patients with Alzheimers Disease

Changes in cerebrospinal fluid (CSF) biomarkers are representative of biochemical changes in the brain. Collection of CSF by lumbar puncture (LP) is essential for biomarker analysis, which is important for research in neurodegenerative disorders. However, LP for research purposes has been controversial due to a reported high incidence of severe LP headache when using standard 18g or 20g Quincke needles with a beveled cutting tip. A procedural safety analysis was performed using the database of a multicenter, 13-week study of CSF cholinesterase activity. A 24g Sprotte atraumatic needle was used to collect CSF at baseline and at Week 13 from 63 older patients with mild to moderate Alzheimer's disease. There was a < 2% LP headache incidence, and a favorable safety profile was reported. In conclusion, LP performed with a 24g Sprotte atraumatic needle (blunt, "bullet" tip) was a well tolerated procedure, with good acceptability.

CSF cholinesterase in early-onset and late-onset Alzheimer's disease and multi-infarct dementia of Chinese patients.

Using Ellman spectrophotometric method we measured the total cholinesterase (ChE) activity in lumbar cerebrospinal fluid (CSF) of 13 persons without neurological disorder, 10 non-demented patients with cerebral infarcts, 17 patients with dementia of Alzheimer's type (DAT) (11 presenile, 6 senile cases), 10 patients with multi-infarct dementia (MID), 1 patient with Parkinson's disease associated with dementia. The ChE activity in CSF was significantly lower in the DAT group compared with age-matched control subjects (p < 0.001). This paper also analyses the possibility of using CSF ChE activity as a marker of DAT, and the relationships between its level of activity and the age of the patient at onset, stage of illness and severity of dementia as well as discrepancies in the data published so far. Previous work has shown that ChE activity in the brain tissue and CSF of MID is normal: therefore, if low ChE activity is found in the CSF of MID patients, as was obtained in 8 out of 10 cases in our series, the diagnosis of mixed dementia should be considered.

CSF cholinesterase activity in demented and non-demented subjects.

Samples of cerebrospinal fluid (CSF) were examined, looking mainly at total cholinesterase (ChE) and acetyl-cholinesterase (AChE) levels from 139 living subjects. At the completion of the study, 35 of the 139 patients had died and pathological confirmation of the presence of dementia had been obtained. These results, together with results from other laboratories, provide evidence that a low CSF ChE level presenting in demented patients may indicate a depletion of the brain AChE system, and this may confirm a clinical diagnosis of AD as well as other types of dementia which are associated with an alteration of the brain AChE system. The overlap in the levels of CSF biochemical markers between demented and non-demented subjects which has led to many conflicting reports has always disappointed investigators. It is suggested that some 'control' subjects with CSF ChE activity indistinguishable from that in AD patients may have an abnormal ageing process in their brains (brain at risk), although the symptoms of dementia have not yet been detected. Recognition of a pre-clinical or incubation period is very beneficial for explaining discrepancies in biochemistry and pathology in the literature, and must be considered for both the treatment and the prevention of dementia. The long used treatment, which was designed to inhibit AChE, should no longer be used: treatment must be designed to enhance the activity of the neuronal AChE system, or slow its degeneration.

Bolus Metoclopramide Does Not Enhance Morphine Analgesia After Cesarean Section

Intravenous metoclopramide potentiates the analgesic effects of opioids in postoperative patients.We speculate that increased spinal concentrations of acetylcholine from metoclopramide-induced acetylcholinesterase inhibition is the mechanism responsible for enhanced morphine analgesia from metoclopramide. Sixty patients undergoing elective cesarean section with subarachnoid anesthesia were randomized to receive either 20 mg metoclopramide or saline intravenously 30-60 min prior to subarachnoid injection. Prior to subarachnoid injection of local anesthetic, 2 mL of cerebrospinal fluid (CSF) was aspirated for cholinesterase activity measurement. Visual analog scale (VAS) scores for pain were obtained prior to drug administration, at first patient request for analgesia, and at discharge from the postanesthesia care unit. Total morphine use was recorded in the recovery room and for 24 h postoperatively. There were no significant differences in VAS scores, morphine use, or CSF cholinesterase activity between groups. CSF cholinesterase activity was similar to values in nonpregnant patients demonstrated previously. This study failed to confirm the morphine-enhancing action of 20 mg intravenous metoclopramide in postoperative patients. Furthermore, this dose of metoclopramide does not inhibit CSF acetylcholinesterase. (Anesth Analg 1996;82:1033-5)

The cerebrospinal fluid choline levels in patients with Huntington's chorea. Negative effect of haloperidol treatment.

Lumbar cerebrospinal fluid (CSF) choline (CH) levels were measured in patients with Huntington's chorea (n = 14). This group was found not to differ significantly from normal controls (n = 13). The values for lumbar CSF Ch levels in the normal subjects were comparable with previously reported values. Of the choreic patients, seven were put on haloperidol treatment (4--6 mg daily). The CSF choline level remained unchanged with this treatment after 20 days. CSF cholinesterase activity was measured in the control and choreic group. The results were not significantly different.

Cholinesterase Activity in Cerebro-Spinal Fluid

THE published finding of Stedman and Stedman1, that cholinesterase cannot be detected in cerebro-spinal fluid, appears to be generally accepted, for recent literature contains no account of further investigations in cholinesterase activity.