12 results on '"Jensen, Rigmor H."'
Search Results
2. Management and Outcome of Pregnancy in Patients With Idiopathic Intracranial Hypertension
- Author
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Vukovic-Cvetkovic, Vlasta, primary, Beier, Dagmar, additional, Buchgreitz, Line, additional, Korsbaek, Johanne J., additional, and Jensen, Rigmor H., additional
- Published
- 2024
- Full Text
- View/download PDF
3. Induction of cluster headache after opening of adenosine triphosphate-sensitive potassium channels:a randomized clinical trial
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Al-Khazali, Haidar M., Deligianni, Christina I., Pellesi, Lanfranco, Al-Karagholi, Mohammad Al Mahdi, Ashina, Håkan, Chaudhry, Basit Ali, Petersen, Anja Sofie, Jensen, Rigmor H., Amin, Faisal Mohammad, Ashina, Messoud, Al-Khazali, Haidar M., Deligianni, Christina I., Pellesi, Lanfranco, Al-Karagholi, Mohammad Al Mahdi, Ashina, Håkan, Chaudhry, Basit Ali, Petersen, Anja Sofie, Jensen, Rigmor H., Amin, Faisal Mohammad, and Ashina, Messoud
- Abstract
Activation of adenosine triphosphate-sensitive potassium (KATP) channels has been implicated in triggering migraine attacks. However, whether the opening of these channels provoke cluster headache attacks remains undetermined. The hallmark of cluster headache is a distinct cyclical pattern of recurrent, severe headache episodes, succeeded by intervals of remission where no symptoms are present. In our study, we enrolled 41 participants: 10 with episodic cluster headaches during a bout, 15 in the attack-free remission period, and 17 diagnosed with chronic cluster headaches. Over 2 distinct experimental days, participants underwent a continuous 20-minute infusion of levcromakalim, a KATP channel opener, or a placebo (isotonic saline), followed by a 90-minute observational period. The primary outcome was comparing the incidence of cluster headache attacks within the postinfusion observation period between the levcromakalim and placebo groups. Six of 10 participants (60%) with episodic cluster headaches in bout experienced attacks after levcromakalim infusion, vs just 1 of 10 (10%) with placebo (P = 0.037). Among those in the remission phase, 1 of 15 participants (7%) reported attacks after levcromakalim, whereas none did postplacebo (P = 0.50). In addition, 5 of 17 participants (29%) with chronic cluster headache had attacks after levcromakalim, in contrast to none after placebo (P = 0.037). These findings demonstrate that KATP channel activation can induce cluster headache attacks in participants with episodic cluster headaches in bout and chronic cluster headache, but not in those in the remission period. Our results underscore the potential utility of KATP channel inhibitors as therapeutic agents for cluster headaches., ABSTRACT: Activation of adenosine triphosphate-sensitive potassium (K ATP ) channels has been implicated in triggering migraine attacks. However, whether the opening of these channels provoke cluster headache attacks remains undetermined. The hallmark of cluster headache is a distinct cyclical pattern of recurrent, severe headache episodes, succeeded by intervals of remission where no symptoms are present. In our study, we enrolled 41 participants: 10 with episodic cluster headaches during a bout, 15 in the attack-free remission period, and 17 diagnosed with chronic cluster headaches. Over 2 distinct experimental days, participants underwent a continuous 20-minute infusion of levcromakalim, a K ATP channel opener, or a placebo (isotonic saline), followed by a 90-minute observational period. The primary outcome was comparing the incidence of cluster headache attacks within the postinfusion observation period between the levcromakalim and placebo groups. Six of 10 participants (60%) with episodic cluster headaches in bout experienced attacks after levcromakalim infusion, vs just 1 of 10 (10%) with placebo ( P = 0.037). Among those in the remission phase, 1 of 15 participants (7%) reported attacks after levcromakalim, whereas none did postplacebo ( P = 0.50). In addition, 5 of 17 participants (29%) with chronic cluster headache had attacks after levcromakalim, in contrast to none after placebo ( P = 0.037). These findings demonstrate that K ATP channel activation can induce cluster headache attacks in participants with episodic cluster headaches in bout and chronic cluster headache, but not in those in the remission period. Our results underscore the potential utility of K ATP channel inhibitors as therapeutic agents for cluster headaches.
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- 2024
4. Compensated Hypogonadism Identified in Males with Cluster Headache:A Prospective Case-Controlled Study
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Petersen, Anja S., Kristensen, David M., Westgate, Connar S. J., Folkmann-Hansen, Thomas, Lund, Nunu, Barloese, Mads, Søborg, Marie Louise K., Snoer, Agneta, Johannsen, Trine H., Frederiksen, Hanne, Juul, Anders, Jensen, Rigmor H., Petersen, Anja S., Kristensen, David M., Westgate, Connar S. J., Folkmann-Hansen, Thomas, Lund, Nunu, Barloese, Mads, Søborg, Marie Louise K., Snoer, Agneta, Johannsen, Trine H., Frederiksen, Hanne, Juul, Anders, and Jensen, Rigmor H.
- Abstract
Objective Androgens have been hypothesized to be involved in the pathophysiology of cluster headache due to the male predominance, but whether androgens are altered in patients with cluster headache remains unclear. Methods We performed a prospective, case-controlled study in adult males with cluster headache. Sera were measured for hormones including testosterone, luteinizing hormone (LH), and sex hormone-binding globulin in 60 participants with episodic cluster headache (during a bout and in remission), 60 participants with chronic cluster headache, and 60 age- and sex-matched healthy controls. Free testosterone (fT) was calculated according to the Vermeulen equation. Shared genetic risk variants were assessed between cluster headache and testosterone concentrations. Results The mean fT/LH ratio was reduced by 35% (95% confidence interval [CI]: 21%–47%, p < 0.0001) in patients with chronic cluster headache and by 24% (95% CI: 9%–37%, p = 0.004) in patients with episodic cluster headache compared to controls after adjusting for age, sleep duration, and use of acute medication. Androgen concentrations did not differ between bouts and remissions. Furthermore, a shared genetic risk allele, rs112572874 (located in the intron of the microtubule associated protein tau (MAPT) gene on chromosome 17), between fT and cluster headache was identified. Interpretation Our results demonstrate that the male endocrine system is altered in patients with cluster headache to a state of compensated hypogonadism, and this is not an epiphenomenon associated with sleep or the use of acute medication. Together with the identified shared genetic risk allele, this may suggest a pathophysiological link between cluster headache and fT. ANN NEUROL 2024, Objective: Androgens have been hypothesized to be involved in the pathophysiology of cluster headache due to the male predominance, but whether androgens are altered in patients with cluster headache remains unclear. Methods: We performed a prospective, case-controlled study in adult males with cluster headache. Sera were measured for hormones including testosterone, luteinizing hormone (LH), and sex hormone-binding globulin in 60 participants with episodic cluster headache (during a bout and in remission), 60 participants with chronic cluster headache, and 60 age- and sex-matched healthy controls. Free testosterone (fT) was calculated according to the Vermeulen equation. Shared genetic risk variants were assessed between cluster headache and testosterone concentrations. Results: The mean fT/LH ratio was reduced by 35% (95% confidence interval [CI]: 21%–47%, p < 0.0001) in patients with chronic cluster headache and by 24% (95% CI: 9%–37%, p = 0.004) in patients with episodic cluster headache compared to controls after adjusting for age, sleep duration, and use of acute medication. Androgen concentrations did not differ between bouts and remissions. Furthermore, a shared genetic risk allele, rs112572874 (located in the intron of the microtubule associated protein tau (MAPT) gene on chromosome 17), between fT and cluster headache was identified. Interpretation: Our results demonstrate that the male endocrine system is altered in patients with cluster headache to a state of compensated hypogonadism, and this is not an epiphenomenon associated with sleep or the use of acute medication. Together with the identified shared genetic risk allele, this may suggest a pathophysiological link between cluster headache and fT. ANN NEUROL 2024.
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- 2024
5. Biomarkers in cluster headache:A systematic review
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Søborg, Marie Louise K., Jensen, Rigmor H., Barloese, Mads, Petersen, Anja S., Søborg, Marie Louise K., Jensen, Rigmor H., Barloese, Mads, and Petersen, Anja S.
- Abstract
Objective To systematically investigate previously examined biomarkers in blood, urine, cerebrospinal fluid, tear fluid, and saliva of patients with cluster headache. Background Cluster headache is a condition with extensive clinical challenges in terms of diagnosis and treatment. Identification of a biomarker with diagnostic implications or as a potential treatment target is highly warranted. Methods We conducted a systematic review including peer reviewed full text of studies that measured biochemical compounds in either blood, urine, cerebrospinal fluid, tear fluid, or saliva of patients with cluster headache diagnosed after the implementation of the International Classification of Headache Disorders (1988) written in English, Danish, Swedish, or Norwegian. Inclusion required a minimum of five participants. The search was conducted in PubMed and EMBASE, in September 2022, and extracted data were screened by two authors. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines for reporting systematic reviews were followed. The Newcastle–Ottawa Scale was used to assess the risk of bias in case–controlled studies. Results We included 40 studies involving 832 patients with cluster headache and 872 controls, evaluating 80 potential biomarkers. The risk of bias for case–controlled studies was a median of 6 (range: 3–8) and 20 studies out of 40 (50%) were of fair or good quality. Most studies were identified within three groups: hypothalamic-regulated hormones, inflammatory markers, and neuropeptides. Among the hypothalamic hormones, cortisol was the most frequently investigated (N = 7) and was elevated in cluster headache in most of the studies. The most frequently examined inflammatory marker was interleukin 1 (N = 3), but findings were divergent. Calcitonin gene–related peptide was the most investigated neuropeptide (N = 9) and all studies found increased levels during attacks. Conclusion B, Objective: To systematically investigate previously examined biomarkers in blood, urine, cerebrospinal fluid, tear fluid, and saliva of patients with cluster headache. Background: Cluster headache is a condition with extensive clinical challenges in terms of diagnosis and treatment. Identification of a biomarker with diagnostic implications or as a potential treatment target is highly warranted. Methods: We conducted a systematic review including peer reviewed full text of studies that measured biochemical compounds in either blood, urine, cerebrospinal fluid, tear fluid, or saliva of patients with cluster headache diagnosed after the implementation of the International Classification of Headache Disorders (1988) written in English, Danish, Swedish, or Norwegian. Inclusion required a minimum of five participants. The search was conducted in PubMed and EMBASE, in September 2022, and extracted data were screened by two authors. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines for reporting systematic reviews were followed. The Newcastle–Ottawa Scale was used to assess the risk of bias in case–controlled studies. Results: We included 40 studies involving 832 patients with cluster headache and 872 controls, evaluating 80 potential biomarkers. The risk of bias for case–controlled studies was a median of 6 (range: 3–8) and 20 studies out of 40 (50%) were of fair or good quality. Most studies were identified within three groups: hypothalamic-regulated hormones, inflammatory markers, and neuropeptides. Among the hypothalamic hormones, cortisol was the most frequently investigated (N = 7) and was elevated in cluster headache in most of the studies. The most frequently examined inflammatory marker was interleukin 1 (N = 3), but findings were divergent. Calcitonin gene–related peptide was the most investigated neuropeptide (N = 9) and all studies found increased levels during attacks. Conclusion: Biomarker findings have been inconsistent and wid
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- 2024
6. CCH attack frequency reduction after psilocybin correlates with hypothalamic functional connectivity
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Madsen, Martin K., Petersen, Anja Sofie, Stenbæk, Dea S., Sørensen, Inger Marie, Schiønning, Harald, Fjeld, Tobias, Nykjær, Charlotte H., Larsen, Sara Marie Ulv, Grzywacz, Maria, Mathiesen, Tobias, Klausen, Ida L., Overgaard-Hansen, Oliver, Brendstrup-Brix, Kristoffer, Linnet, Kristian, Johansen, Sys S., Fisher, Patrick M., Jensen, Rigmor H., Knudsen, Gitte M., Madsen, Martin K., Petersen, Anja Sofie, Stenbæk, Dea S., Sørensen, Inger Marie, Schiønning, Harald, Fjeld, Tobias, Nykjær, Charlotte H., Larsen, Sara Marie Ulv, Grzywacz, Maria, Mathiesen, Tobias, Klausen, Ida L., Overgaard-Hansen, Oliver, Brendstrup-Brix, Kristoffer, Linnet, Kristian, Johansen, Sys S., Fisher, Patrick M., Jensen, Rigmor H., and Knudsen, Gitte M.
- Abstract
Objective: To evaluate the feasibility and prophylactic effect of psilocybin as well as its effects on hypothalamic functional connectivity (FC) in patients with chronic cluster headache (CCH). Background: CCH is an excruciating and difficult-to-treat disorder with incompletely understood pathophysiology, although hypothalamic dysfunction has been implicated. Psilocybin may have beneficial prophylactic effects, but clinical evidence is limited. Methods: In this small open-label clinical trial, 10 patients with CCH were included and maintained headache diaries for 10 weeks. Patients received three doses of peroral psilocybin (0.14 mg/kg) on the first day of weeks five, six, and seven. The first 4 weeks served as baseline and the last 4 weeks as follow-up. Hypothalamic FC was determined using functional magnetic resonance imaging the day before the first psilocybin dose and 1 week after the last dose. Results: The treatment was well tolerated. Attack frequency was reduced by mean (standard deviation) 31% (31) from baseline to follow-up (pFWER = 0.008). One patient experienced 21 weeks of complete remission. Changes in hypothalamic–diencephalic FC correlated negatively with a percent change in attack frequency (pFWER = 0.03, R = −0.81), implicating this neural pathway in treatment response. Conclusion: Our results indicate that psilocybin may have prophylactic potential and implicates the hypothalamus in possible treatment response. Further clinical studies are warranted.
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- 2024
7. Induction of cluster headache after opening of adenosine triphosphate-sensitive potassium channels: a randomized clinical trial.
- Author
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Al-Khazali, Haidar M., Deligianni, Christina I., Pellesi, Lanfranco, Al-Karagholi, Mohammad Al-Mahdi, Ashina, Håkan, Chaudhry, Basit Ali, Petersen, Anja Sofie, Jensen, Rigmor H., Amin, Faisal Mohammad, and Ashina, Messoud
- Published
- 2024
- Full Text
- View/download PDF
8. CCH attack frequency reduction after psilocybin correlates with hypothalamic functional connectivity
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Madsen, Martin K., primary, Petersen, Anja Sofie, additional, Stenbæk, Dea S., additional, Sørensen, Inger Marie, additional, Schiønning, Harald, additional, Fjeld, Tobias, additional, Nykjær, Charlotte H., additional, Larsen, Sara Marie Ulv, additional, Grzywacz, Maria, additional, Mathiesen, Tobias, additional, Klausen, Ida L., additional, Overgaard‐Hansen, Oliver, additional, Brendstrup‐Brix, Kristoffer, additional, Linnet, Kristian, additional, Johansen, Sys S., additional, Fisher, Patrick M., additional, Jensen, Rigmor H., additional, and Knudsen, Gitte M., additional
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- 2024
- Full Text
- View/download PDF
9. Spontaneous Intracranial Hypotension: Long-Term Follow-Up.
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Vukovic-Cvetkovic, Vlasta, Schytz, Henrik W., Smilkov, Emil Andonov, and Jensen, Rigmor H.
- Subjects
HYPOTENSION ,INTRACRANIAL pressure ,AGE of onset ,DISEASE duration - Abstract
The outcome of spontaneous intracranial hypotension (SIH) years after onset is largely unknown. The objective of our study was to describe our clinical experience and long-term outcomes in a case series of patients with SIH. From March 2007 to March 2022, demographic variables, clinical symptoms, neuroimaging findings, and response to treatment were retrospectively analyzed in patients with confirmed SIH and in a subgroup of patients with clinical symptoms but not confirmed by MR or LP, probable SIH (pSIH). We have included 37 SIH and 13 pSIH patients. The average age at onset was 44 years, and 59% (pSIH 46%) were women. All patients presented with a new-onset orthostatic headache. In the SIH group, brain MRI showed signs of intracranial hypotension in all patients, spinal MR was performed in 70%, and pathological findings were identified in 73%. The range of EBP was 1-8 (average 2.2). Good outcome after single or 2 EBPs had 42% (pSIH 46%) of patients. At follow-up, 81% (pSIH 54%) of patients had a favorable outcome. Relapse occurred in 16% of patients in the SIH group and none in the pSIH group. The mean follow-up time was 60 months. EBP is an effective and minimally invasive treatment, and efficacy seems independent of disease duration. The long-term prognosis is favorable in 80% of SIH patients and in half of pSIH patients. Despite the lack of MRI signs of low intracranial pressure on neuroimaging, pSIH patients should also be offered EBP, and more awareness of SIH is needed. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
- View/download PDF
10. Biomarkers in cluster headache: A systematic review.
- Author
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Søborg, Marie‐Louise K., Jensen, Rigmor H., Barloese, Mads, and Petersen, Anja S.
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BIOMARKERS , *PROFESSIONAL peer review , *ONLINE information services , *NOSOLOGY , *MEDICAL information storage & retrieval systems , *SALIVA , *NEUROPEPTIDES , *SYSTEMATIC reviews , *CASE-control method , *HYPOTHALAMIC hormones , *INTERLEUKIN-1 , *CALCITONIN , *TEARS (Body fluid) , *RESEARCH funding , *DESCRIPTIVE statistics , *CLUSTER headache , *CEREBROSPINAL fluid , *MEDLINE , *RESEARCH bias , *HYDROCORTISONE - Abstract
Objective: To systematically investigate previously examined biomarkers in blood, urine, cerebrospinal fluid, tear fluid, and saliva of patients with cluster headache. Background: Cluster headache is a condition with extensive clinical challenges in terms of diagnosis and treatment. Identification of a biomarker with diagnostic implications or as a potential treatment target is highly warranted. Methods: We conducted a systematic review including peer reviewed full text of studies that measured biochemical compounds in either blood, urine, cerebrospinal fluid, tear fluid, or saliva of patients with cluster headache diagnosed after the implementation of the International Classification of Headache Disorders (1988) written in English, Danish, Swedish, or Norwegian. Inclusion required a minimum of five participants. The search was conducted in PubMed and EMBASE, in September 2022, and extracted data were screened by two authors. Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines for reporting systematic reviews were followed. The Newcastle–Ottawa Scale was used to assess the risk of bias in case–controlled studies. Results: We included 40 studies involving 832 patients with cluster headache and 872 controls, evaluating 80 potential biomarkers. The risk of bias for case–controlled studies was a median of 6 (range: 3–8) and 20 studies out of 40 (50%) were of fair or good quality. Most studies were identified within three groups: hypothalamic‐regulated hormones, inflammatory markers, and neuropeptides. Among the hypothalamic hormones, cortisol was the most frequently investigated (N = 7) and was elevated in cluster headache in most of the studies. The most frequently examined inflammatory marker was interleukin 1 (N = 3), but findings were divergent. Calcitonin gene–related peptide was the most investigated neuropeptide (N = 9) and all studies found increased levels during attacks. Conclusion: Biomarker findings have been inconsistent and widely non‐specific for cluster headache, which explains why none of the previous studies succeeded in identifying a unique biomarker for cluster headache, but instead contributed to substantiating the underlying pathophysiologic mechanisms. Several of the examined biomarkers could hold promise as markers for disease activity but are unfit for a clear distinction from both controls and other headaches. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
- View/download PDF
11. Recent advances in diagnosing, managing, and understanding the pathophysiology of cluster headache.
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Petersen, Anja S, Lund, Nunu, Goadsby, Peter J, Belin, Andrea C, Wang, Shuu-Jiun, Fronczek, Rolf, Burish, Mark, Cho, Soo-Jin, Peres, Mario F P, and Jensen, Rigmor H
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CLUSTER headache , *CALCITONIN gene-related peptide , *PRIMARY headache disorders , *DIAGNOSIS , *PATHOLOGICAL physiology - Abstract
Cluster headache, characterised by attacks of severe, recurrent, unilateral headache and ipsilateral cranial autonomic symptoms, remains a primary headache with an elusive pathophysiology. Recent advances have introduced effective treatments and broadened understanding of the clinical features of cluster headache. These features are similar in patients globally, but regional differences in prevalence and burden exist. International collaborations have led to identification of eight genetic loci associated with cluster headache. The pathophysiological mechanisms are still not fully understood but recent studies show that targeting the trigeminal autonomic reflex by neurostimulation, or targeting the neuropeptide calcitonin gene-related peptide (CGRP), might lessen the attack burden. The US Food and Drug Administration has approved galcanezumab, a monoclonal antibody targeting CGRP, as the first specific preventive treatment for episodic cluster headache. However, a preventive effect was not replicated in chronic cluster headache, and the European Medicines Agency did not approve galcanezumab, restricting its availability in Europe. Owing to the low prevalence of cluster headache, continued collaboration through multicentre clinical trials and data sharing will be imperative for further breakthroughs in understanding and management. [ABSTRACT FROM AUTHOR]
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- 2024
- Full Text
- View/download PDF
12. The impact of eating disorders on idiopathic intracranial hypertension.
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Wallentin, Therese, Linnet, Jakob, Lichtenstein, Mia B, Hansen, Nadja S, Korsbæk, Johanne J, Høgedal, Lisbeth, Hagen, Snorre M, Molander, Laleh D, Jensen, Rigmor H, and Beier, Dagmar
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INTRACRANIAL hypertension , *EATING disorders , *CHILDBEARING age , *VISUAL fields , *OPTIC nerve - Abstract
Background: Idiopathic intracranial hypertension (IIH) occurs more frequently in obese females of childbearing age. A link between eating disorders and poor outcome has been suggested but remains unproven. Methods: This prospective field study at two tertiary headache centers included patients with clinically suspected IIH after standardized diagnostic work-up. Eating disorders were evaluated using validated questionnaires (EDQs). Primary outcome was the impact of eating disorders on IIH severity and outcome, secondary outcome was the prevalence and type of eating disorders in IIH compared to controls. Results: We screened 326 patients; 143 patients replied to the EDQs and were classified as 'IIH' or 'non-IIH' patients. The demographic profile of EDQ-respondents and non-respondents was similar. Presence of an eating disorder did not impact IIH severity (lumbar puncture opening pressure (p = 0.63), perimetric mean deviation (p = 0.18), papilledema (Frisén grad 1–3; p = 0.53)) nor IIH outcome (optic nerve atrophy (p = 0.6), impaired visual fields (p = 0.18)). Moreover, we found no differences in the prevalence and type of eating disorders when comparing IIH with non-IIH patients (p = 0.09). Conclusion: Eating disorders did not affect IIH severity or outcome. We found the same prevalence and distribution pattern of eating disorders in IIH and non-IIH patients advocating against a direct link between IIH and eating disorders. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
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