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Background: Although headache is the most common complication of dural puncture, knowledge gaps remain about patient-related risks. Data are lacking on the role, if any, of tobacco smoking, race, anxiety, depression, and Post Traumatic Stress Disorder (PTSD) in conferring risk for post-dural puncture headache (PDPH). Objective: To determine the influence of tobacco smoking, race, anxiety, depressed mood, and PTSD on the risk for PDPH. Study Design: Retrospective chart review, single site. Methods: We determined the incidence of significant PDPH according to age, sex, race, smoking status, and psychiatric diagnosis in 153 consecutive research patients at the Cincinnati Veterans Affairs Medical Center who had continuous cerebrospinal fluid (CSF) sampling performed after using a largebore (17 gauge) Tuohy needle to place a 20-gauge polyamide catheter in the lumbar spinal canal. Results: Thirty-nine subjects (25.5%) had significant PDPH, defined as requiring an epidural blood patch for therapy (an average of 4 days post-procedure). Greater age was associated with a decreased risk of PDPH (P = 0.008); subjects over the age of 40 had the lowest incidence (15.7%). Women and men had a 31.4% and 23.7% incidence of PDPH, respectively; these were not significantly different (P = 0.38). Neither were rates of PDPH in Caucasians (28.0%) and AfricanAmericans (15.6%) significantly different (P = 0.18). Healthy controls had a higher incidence of PDPH than patients with PTSD (P = 0.032). Smokers had a lower incidence of PDPH than nonsmokers, 13.7% vs. 34.1% (P = 0.009). Limitations: This was not a prospective study, rather a retrospective chart review. Conclusion: Most notably, smokers had a considerably reduced rate of PDPH in comparison with non-smokers. This information could be a useful addition to the clinical assessment of relative risk for PDPH. Further research into the mechanisms by which tobacco smoking may inhibit PDPH, such as nicotine stimulation of dopamine neurotransmission or alterations in coagulation, appears warranted. Key words: Anxiety, cerebrospinal fluid (CSF), epidural blood patch, headache, lumbar puncture, pain, post-dural puncture headache, post-traumatic stress disorder (PTSD), race, tobacco, Tuohy needle

Accruing evidence indicates that neuropeptide Y (NPY), a peptide neurotransmitter, is a resilience-to-stress factor in humans. We previously reported reduced cerebrospinal fluid (CSF) NPY concentrations in combat-related posttraumatic stress disorder (PTSD) subjects as compared with healthy, non-combat-exposed volunteers. Here we report CSF NPY in combat-exposed veterans with and without PTSD. We quantified NPY concentrations in morning CSF from 11 male subjects with PTSD from combat in Iraq and/or Afghanistan and from 14 combat-exposed subjects without PTSD. NPY-like immunoreactivity (NPY-LI) was measured by EIA. The relationship between CSF NPY and clinical symptoms, as measured by the Clinician-Administered PTSD Scale (CAPS) and Beck Depression Inventory (BDI), was assessed, as was the relationship between combat exposure scale (CES) scores and CSF NPY. As compared with the combat-exposed comparison subjects without PTSD, individuals with PTSD had significantly lower concentrations of CSF NPY [mean CSF NPY was 258.6 ± 21.64 pg/mL in the combat trauma-no PTSD group but only 180.5 ± 12.62 pg/mL in PTSD patients (p = 0.008)]. After adjusting for CES and BDI scores the two groups were still significantly different with respect to NPY. Importantly, CSF NPY was negatively correlated with composite CAPS score and intrusive (re-experiencing) subscale scores, but did not significantly correlate with CES or BDI scores. Our current findings further suggest that NPY may regulate the manifestation of PTSD symptomatology, and extend previous observations of low CSF NPY concentrations in the disorder. Central nervous system NPY may be a clinically important pharmacotherapeutic target, and/or diagnostic measure, for PTSD.

Although headache is the most common complication of dural puncture, knowledge gaps remain about patient-related risks. Data are lacking on the role, if any, of tobacco smoking, race, anxiety, depression, and Post Traumatic Stress Disorder (PTSD) in conferring risk for post-dural puncture headache (PDPH). To determine the influence of tobacco smoking, race, anxiety,depressed mood, and PTSD on the risk for PDPH. Retrospective chart review, single site. We determined the incidence of significant PDPH according to age, sex, race, smoking status, and psychiatric diagnosis in 153 consecutive research patients at the Cincinnati Veterans Affairs Medical Center who had continuous cerebrospinal fluid (CFS) sampling performed after using a large-bore (17 gauge) Tuohy needle to place a 20-gauge polyamide catheter in the lumbar spinal canal. Thirty-nine subjects (25.5%) had significant PDPH, defined as requiring an epidural blood patch for therapy (an average of 4 days post-procedure). Greater age was associated with a decreased risk of PDPH (P = 0.008); subjects over the age of 40 had the lowest incidence (15.7%). Women and men had a 31.4% and 23.7% incidence of PDPH, respectively; these were not significantly different (P = 0.38). Neither were rates of PDPH in Caucasians (28.0%) and African-Americans (15.6%) significantly different (P = 0.18) Healthy controls had a higher incidence of PDPH than patients with PTSD (P = 0.032). Smokers had a lower incidence of PDPH than non-smokers, 13.7% vs. 34.1% (P = 0.009). This was not a prospective study, rather a retrospective chart review. Most notably, smokers had a considerably reduced rate of PDPH in comparison with non-smokers. This information could be a useful addition to the clinical assessment of relative risk for PDPH. Further research into the mechanisms by which tobacco smoking may inhibit PDPH, such as nicotine stimulation of dopamine neurotransmission or alterations in coagulation, appears warranted.

Dopaminergic mechanisms may be involved in the pathophysiology of posttraumatic stress disorder (PTSD), although the evidence for this is limited; serotonergic mechanisms are implicated largely by virtue of the modest efficacy of serotonergic drugs in the treatment of the disorder. Basal cerebrospinal fluid (CSF) dopamine and serotonin metabolite concentrations are normal in PTSD patients. However, in the present experiment, we postulated that perturbations in CSF dopamine and serotonin metabolites could be induced by acute psychological stress. Ten volunteers with war-related chronic PTSD underwent 6-h continuous lumbar CSF withdrawal on two occasions per patient (6-9 weeks apart), using a randomized, within subject-controlled, crossover design. During one session a 1-h video with trauma-related footage (traumatic video) was shown and in the other session subjects viewed a 1-h neutral video. We quantified the dopamine metabolite homovanillic acid (HVA) and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in CSF at 10-min intervals, before, during, and after video provocation. Blood pressure, heart rate, and subjective anxiety and mood were monitored. Significant drop in mood and increases in anxiety and blood pressure occurred during the traumatic relative to the neutral movie. CSF HVA concentrations diminished significantly after the traumatic video (p 0.05), in comparison with the neutral, while 5-HIAA tended to diminish (p 0.10). We conclude that an acute decline in CNS HVA concentrations is associated with laboratory-induced symptoms in chronic PTSD patients. While further research is required to determine if the stress-induced dopaminergic changes are normative or pathological, the present data suggest that increasing dopaminergic neurotransmission be explored as a potential therapy, or adjunctive therapy, for PTSD.