Levels Of Cerebrospinal Fluid Somatostatin Research Articles

Glial Cell Line-Derived Neurotrophic Factor and Somatostatin Levels in Cerebrospinal Fluid of Patients Affected by Chronic Migraine and Fibromyalgia

The aim of the present study was to verify cerebrospinal fluid (CSF) levels of glial cell line-derived neurotrophic factor (GDNF) and somatostatin, both measured by sensitive immunoassay, in: 16 chronic migraine (CM) patients, 15 patients with an antecedent history of migraine without aura diagnosed as having probable chronic migraine (PCM) and probable analgesic-abuse headache (PAAH), 20 patients affected by primary fibromyalgia syndrome (PFMS), and 20 control subjects. Significantly lower levels of GDNF and somatostatin were found in the CSF of both CM and PCM + PAAH patients compared with controls (GDNF =P < 0.001, P < 0.002; somatostatin = P < 0.002, P < 0.0003), without significant difference between the two groups. PFMS patients, with and without analgesic abuse, also had significantly lower levels of both somatostatin and GDNF (P < 0.0002, P < 0.001), which did not differ from those of CM and PCM + PAAH patients. A significant positive correlation emerged between CSF values of GDNF and those of somatostatin in CM (r = 0.70, P < 0.02), PCM + PAAH (r = 0.78, P < 0.004), and PFMS patients (r = 0.68, P < 0.008). Based on experimental findings, it can be postulated that reduced CSF levels of GDNF and somatostatin in both CM and PCM + PAAH patients can contribute to sustained central sensitization underlying chronic head pain. The abuse of simple or combination analgesics does not seem to influence the biochemical changes investigated, which appear to be more strictly related to the chronic pain state, as demonstrated also for fibromyalgia.

Cerebrospinal fluid somatostatin levels in febrile seizures and epilepsy in children

We analysed the level of cerebrospinal fluid (CSF) somatostatin in children with febrile seizures and epilepsy. In the febrile seizure group (n = 23), the somatostatin level was 83.9 ± 11.2 pg/ml, which was significantly higher than that of age-matched controls. CSF samples obtained within 3 h of the last seizure had higher somatostatin levels (106.1 ± 12.4 pg/ml;n = 14) than did the CSF obtained after 3 h (49.4 ± 15.6 pg/ml;n = 9). The mean somatostatin level in the epilepsy group was 35.3 ± 4.3 pg/ml (n = 34), and was distributed as follows: 27.6 ± 3.6 pg/ml in the idiopathic generalized epilepsy group (n = 16), 44.0 ± 9.4 pg/ml in the symptomatic generalized epilepsy group (n = 13), and 37.2 ± 10.1 pg/ml in the partial epilepsy group (n = 5). The levels in each group were significantly higher than those in age-matched controls. Somatostatin is a hypothalamic tetradecapeptide with excitatory effects on neurons in children with febrile seizures and epilepsy. The finding that patients with convulsive disease had elevated levels of CSF somatostatin suggests that somatostatin release is somehow related to seizure activity. It remains to be determined whether this is due to increased release from over-active excitatory neurons or leakage from damaged or anoxic neurons, secondary to seizure activity.

Neuropeptides in Cerebrospinal Fluid in Normal-Pressure Hydrocephalus and Dementia

Delta-sleep-inducing peptide (DSIP), vasoactive intestinal peptide (VIP), peptide YY (PYY) and somatostatin (SOM) were assayed with specific radioimmunological methods in cerebrospinal fluid (CSF) of healthy volunteers, 12 patients with Alzheimer's disease (AD), 11 patients with multi-infarct dementia (MID) and 10 patients with normal-pressure hydrocephalus (NPH). Patients with NPH were reinvestigated 3 months after a ventriculoperitoneal shunt operation. DSIP, PYY and SOM levels in CSF were decreased in patients with NPH compared to controls. The CSF concentration of SOM was also significantly reduced in patients with AD. No correlations were found between the degree of dementia in any of the illnesses and the CSF concentrations of the peptides. The concentration of DSIP, VIP and SOM increased significantly in parallel to the clinical improvement after the shunt operation in NPH patients.

Reduced Lumbar Cerebrospinal Fluid Somatostatin Levels in Alzheimer's Disease and Dementia with Frontotemporal Degeneration

The present study evaluates the cerebrospinal fluid levels of somatostatin-like immunoreactivity (LI) in two types of primary degenerative dementias: dementia of Alzheimer''s disease (DAT) and dementia with frontotemporal cortical degeneration of non-Alzheimer type (which included Pick''s disease). Several studies have documentated reduced concentration of somatostatin-LI in the brain and cerebrospinal fluid (CSF) in DAT. This study confirmed these results and showed in addition reduced CSF levels of somatostatin-LI in frontal lobe dementia (FTD), which has not been shown previously. There was no significant correlation with the duration of the disease. The histopathology and distribution of cortical degeneration in DAT and FTD differs in most aspects but shares the reduction in somatostatin-LI reduction. This suggests involvement of somatostatin neurons in these two types of primary degenerative dementias.

Effective pharmacotherapy of alcoholic amnestic disorder with fluvoxamine. Preliminary findings

• Ten patients with alcoholic chronic organic brain disease were categorized as having alcohol amnestic disorder, or Korsakoff's psychosis (n = 6), dementia associated with alcoholism (n = 3), or compensated alcoholic liver disease (n =1). All patients had severe deficits in memory for recently acquired information (episodic memory). Patients with alcohol dementia also showed global intellectual decline, including decreased performance on measures of semantic (knowledge) memory and reduction in levels of cerebrospinal fluid somatostatin. In a 4-week double-blind crossover design, the serotonin-uptake blocker fluvoxamine maleate (100 to 200 mg/d) was found to improve episodic memory in only the patients with alcohol amnestic disorder. These improvements in memory were significantly correlated with reductions in levels of cerebrospinal fluid 5-hydroxyindoleacetic acid, suggesting that facilitation of serotonergic neurotransmission may ameliorate the episodic memory failure in patients with alcohol amnestic disorder.

Effective Pharmacotherapy of Alcoholic Amnestic Disorder With Fluvoxamine

Ten patients with alcoholic chronic organic brain disease were categorized as having alcohol amnestic disorder, or Korsakoff's psychosis (n = 6), dementia associated with alcoholism (n = 3), or compensated alcoholic liver disease (n = 1). All patients had severe deficits in memory for recently acquired information (episodic memory). Patients with alcohol dementia also showed global intellectual decline, including decreased performance on measures of semantic (knowledge) memory and reduction in levels of cerebrospinal fluid somatostatin. In a 4-week double-blind crossover design, the serotonin-uptake blocker fluvoxamine maleate (100 to 200 mg/d) was found to improve episodic memory in only the patients with alcohol amnestic disorder. These improvements in memory were significantly correlated with reductions in levels of cerebrospinal fluid 5-hydroxyindoleacetic acid, suggesting that facilitation of serotonergic neurotransmission may ameliorate the episodic memory failure in patients with alcohol amnestic disorder.

Brain and CSF somatostatin concentrations in patients with psychiatric or neurological illness. An overview.

Somatostatin was originally isolated as a 14-amino-acid peptide from the ovine hypothalamus. The peptide has a widespread regional distribution within the central and peripheral nervous systems, as well as in peripheral organs. Preservation of the chemical structure over a wide range of vertebral species indicates important functional roles of the peptide. Recent results about the role of somatostatin and related peptides in different psychiatric (depression, schizophrenia, Alzheimer's disease) and neurological (Huntington's disease, multiple sclerosis, Parkinson's disease) diseases, and the effects on the hypothalamic-pituitary-adrenal axis are summarized. Also, the influence of some psychotropic drugs (halo-peridol, carbamazepine) on somatostatin levels in cerebrospinal fluid is discussed.

CSF somatostatin and abnormal response to dexamethasone administration in schizophrenic and depressed patients.

Low levels of cerebrospinal fluid (CSF) somatostatin and abnormal response to dexamethasone are two neuroendocrine disturbances reported to appear in depression and other neuropsychiatric disorders. We measured the levels of CSF somatostatin in patients with schizophrenia (n = 44) and depression (n = 19). In view of in vitro and animal evidence of the ability of somatostatin to inhibit stimulated corticotropin secretion, we also administered the dexamethasone suppression test to a subgroup of the patients with schizophrenia (n = 16) and the total depressed group. Lower levels of CSF somatostatin were found in dexamethasone nonsuppressors regardless of diagnosis and were negatively correlated with maximum postdexamethasone cortisol level in the total and depressed patient groups. These data suggest a functional relationship between hypothalamic-pituitary-adrenal axis hyperactivity and reduced CSF somatostatin level.

Cerebrospinal fluid vasopressin, oxytocin, somatostatin, and beta-endorphin in Alzheimer's disease.

As a first step toward assessing the status of brain neuropeptide systems that may be involved in Alzheimer's disease (AD), the cerebrospinal fluid (CSF) concentrations of the neuropeptides arginine vasopressin, somatostatin, oxytocin, and beta-endorphin were measured in patients with AD, normal elderly subjects, and normal young subjects. The plasma arginine vasopressin level was also measured in the three groups. The CSF arginine vasopressin level was significantly lower in patients with AD than in either elderly or young normal subjects, but oxytocin and beta-endorphin levels did not differ between groups. The CSF osmolarity also did not differ between groups. The plasma arginine vasopressin level did not significantly differ between groups, but high plasma arginine vasopressin values were absent in the patients with AD. The CSF somatostatin level was significantly lower in patients with AD than in normal elderly persons, but it did not differ in young normal subjects. These results suggest that central vasopressinergic activity may be decreased in AD and confirm reports of low CSF somatostatin levels in AD.

CSF somatostatin in affective illness and normal volunteers

1. 1. Somatostatin is a hypothalamic tetradecapeptide with many central nervous system actions. 2. 2. We investigated a potential role for altered Somatostatin activity in affective disorder by measuring somatostatin in the cerebrospinal fluid (CSF) of 47 patients with affective disorder and of 39 normal volunteers. 3. 3. Medication-free depressed patients showed significantly lower levels of CSF Somatostatin than normal volunteers (p < .001) or patients during the improved state (p < .01). 4. 4. Somatostatin levels were significantly and inversely correlated with duration of sleep on the night of the lumbar puncture (p < .05). 5. 5. Treatment with carbamazepine reduced CSF Somatostatin (p < .01) in contrast to the absence of effect of imipramine, desmethyl imipramine, and lithium carbonate and the significant increase in CSF Somatostatin seen in a small group of patients treated with zimelidine. 6. 6. The implications of these findings with respect to attempts to explore the neurobiology of depression are discussed.

The effect of intravenous growth hormone infusion on cerebrospinal fluid somatostatin levels in the rhesus monkey

CSF was continuously withdrawn over 13 days from the cervical subarachnoid space of two rhesus monkeys during the intravenous infusion of saline or human growth hormone (GH) and samples collected during sequential 2 h periods were assayed for somatostatin (SRIF). SRIF-like immunoreactivity (SRIF-LI) concentrations were decreased during GH infusion as compared to saline infusion ( P < 0.005) and the maximal effect occurred during the hours of darkness (18.00–06.00 h). Since in vivo GH administration stimulates hypothalamic SRIF-LI release, CSF SRIF-LI does not appear to be derived primarily from the hypothalamus but rather from extrahypothalamic brain by a mechanism inhibited by GH.