Potential effects of a mobile stroke unit on time to treatment and outcome in patients treated with thrombectomy or thrombolysis: A Danish-German cross-border analysis.

BACKGROUND AND PURPOSE: A mobile stroke unit (MSU) reduces delays in stroke treatment by allowing thrombolysis on board and avoiding secondary transports. Due to the beneficial effect in comparison to conventional emergency medical services, current guidelines recommend regional evaluation of MSU implementation. METHODS: In a descriptive study, current pathways of patients requiring a secondary transport for mechanical thrombectomy were reconstructed from individual patient records within a Danish (n = 122) and an adjacent German region (n = 80). Relevant timestamps included arrival times (on site, primary hospital, thrombectomy centre) as well as the initiation of acute therapy. An optimal MSU location for each region was determined. The resulting time saving was translated into averted disability-adjusted life years (DALYs). RESULTS: For each region, the optimal MSU location required a median driving time of 35 min to a stroke patient. Time savings in the German region (median [Q1; Q3]) were 7 min (-15; 31) for thrombolysis and 35 min (15; 61) for thrombectomy. In the Danish region, the corresponding time savings were 20 min (8; 30) and 43 min (25; 66). Assuming 28 thrombectomy cases and 52 thrombolysis cases this would translate to 9.4 averted DALYs per year justifying an annual net MSU budget of $0.8M purchasing power parity dollars (PPP-$) in the German region. In the Danish region, the MSU would avert 17.7 DALYs, justifying an annual net budget of PPP-$1.7M. CONCLUSION: The effects of an MSU can be calculated from individual patient pathways and reflect differences in the hospital infrastructure between Denmark and Germany.

Is the TOAST Classification Suitable for Use in Personalized Medicine in Ischemic Stroke?

Pathophysiologic classification of ischemic stroke is essential to a personalized approach to stroke treatment. The Trial of Org 101072 in Acute Stroke Treatment (TOAST) classification is the most frequently used tool to classify index ischemic strokes. We aimed to assess presence of small and large vessel disease markers across the TOAST groups. In an observational study, 99 ischemic stroke patients were consecutively included and classified according to TOAST. The assessment was supplemented with cerebral small vessel disease (SVD) score, based on Magnetic Resonance Imaging (MRI), and tests for carotid atherosclerosis, ankle−brachial index (ABI), estimated glomerular filtration rate (eGFR), and peripheral reactive hyperemia index (RHI). Markers of small and large vessel disease were present in all TOAST groups. Carotid stenosis and atrial fibrillation were associated with their respective TOAST groups (p = 0.023 and p < 0.001, respectively). We found no association between the SVD score and the small vessel occlusion TOAST group (p = 0.59), and carotid atherosclerosis (p = 0.35), RHI (p = 0.39), ABI (p = 0.20), and eGFR (p = 0.79) were not associated with TOAST groups. The TOAST classification does not provide differential information on the pathophysiologies of the ischemic stroke. An operational classification that contains quantification of each vascular pathophysiology in the individual patient is pivotal for future research and development of personalized medicine.

Sleep-disordered breathing and cerebral small vessel disease-acute and 6 months after ischemic stroke.

PURPOSE: Sleep-disordered breathing (SDB) occurs frequently after stroke and is associated with poor functional outcome and increased mortality. The purpose of this study was to detect changes in SDB over time after acute ischemic stroke and investigate relationships between SDB and stroke etiologies with focus on cerebral small vessel disease. METHODS: From May 2015 to August 2016, we conducted an observational study of 99 patients with mild to moderate stroke (median age: 68 years, range 36-88; 56% men). Polysomnography was performed within 7 days of stroke onset (n = 91) and after 6 months (n = 52). The strokes were classified using the etiological TOAST classification. Total small vessel disease (SVD) scores were calculated based on MRIs. RESULTS: SDB, defined as an apnea-hypopnea index (AHI) ≥ 15, was found in 56% of patients in the acute state and in 44% at follow-up. AHI decreased over time (median change 4.7, 95% confidence interval [95% CI] 0.5-8.9; p = 0.03). Patients with AHI ≥ 15 in both the acute state and at follow-up had higher SVD score at follow-up (p = 0.003). AHI was not associated with ischemic stroke subgroups according to the TOAST classification. DISCUSSION: In conclusion, 6 months after stroke, AHI decreased, but 44% still had AHI ≥ 15. Persistent SDB in both the acute state and at follow-up was associated with a higher SVD score, but not to the TOAST subgroups. SDB evaluation should be offered to stroke patients, and the effect of SDB on cerebral small vessel disease needs to be further investigated using the well-defined SVD score. TRIAL REGISTRATION: clinicaltrials.gov NCT02111408, April 11, 2014.

Investigation of cortical thickness and volume during spontaneous attacks of migraine without aura: a 3-Tesla MRI study.

BACKGROUND: Structural imaging has revealed changes in cortical thickness in migraine patients compared to healthy controls is reported, but presence of dynamic cortical and subcortical changes during migraine attack versus inter-ictal phase is unknown. The aim of the present study was to investigate possible changes in cortical thickness during spontaneous migraine attacks. We hypothesized that pain-related cortical area would be affected during the attack compared to an inter-ictal phase. METHODS: Twenty-five patients with migraine without aura underwent three-dimensional T1-weighted imaging on a 3-Tesla MRI scanner during spontaneous and untreated migraine attacks. Subsequently, 20 patients were scanned in the inter-ictal phase, while 5 patients did not show up for the inter-ictal scan. Four patients were excluded from the analysis because of bilateral migraine pain and another one patient was excluded due to technical error in the imaging. Longitudinal image processing was done using FreeSurfer. Repeated measures ANOVA was used for statistical analysis and to control for multiple comparison the level of significance was set at p = 0.025. RESULTS: In a total of 15 patients, we found reduced cortical thickness of the precentral (p = 0.023), pericalcarine (p = 0.024), and temporal pole (p = 0.017) cortices during the attack compared to the inter-ictal phase. Cortical volume was reduced in prefrontal (p = 0.018) and pericalcarine (p = 0.017) cortices. Hippocampus volume was increased during attack (p = 0.007). We found no correlations between the pain side or any other clinical parameters and the reduced cortical size. CONCLUSION: Spontaneous migraine attacks are accompanied by transient reduced cortical thickness and volume in pain-related areas. The findings constitute a fingerprint of acute pain in migraine patients, which can be used as a possible biomarker to predict antimigraine treatment effect in future studies. TRIAL REGISTRATION: The study was registered at ClinicalTrials.gov ( NCT02202486 ).

[Carbon monoxide poisoning and development of delayed neuropsychiatric syndrome in a 77-year-old woman].

This case report describes carbon monoxide (CO) poisoning in a woman. CO is a toxic, odourless and colourless gas. Delayed cognitive sequelae have been described in up to 40% of patients with significant CO poisoning. A 77-year-old woman suffered from severe smoke- and CO poisoning and received hyperbaric O2 therapy, but she continued to have memory impairment and unsteady gait at day 26. Brain MRI showed diffuse white matter lesions in both hemispheres with increased signal on diffusion-weighted imaging. Diagnosis, pathogenesis and treatment of CO poisoning are discussed.

Identical Horner Syndrome in Homozygotic Twins Caused by Non-Traumatic Internal Carotid Artery Dissection.

Internal carotid artery dissection is an uncommon entity and the result of a spontaneous or traumatic tear in the vessel lining. We present two almost identical cases of Horner syndrome caused by spontaneous, non-traumatic internal carotid artery dissection within 4 months in two 52-year-old homozygotic twin brothers.

Favourable prognosis of trigeminal neuralgia when enrolled in a multidisciplinary management program - a two-year prospective real-life study.

BACKGROUND: Prognosis of medically treated trigeminal neuralgia patients is assumed to be poor, but the evidence is lacking. Thus, prospective real-life studies of medical management of trigeminal neuralgia are warranted. METHODS: This was an observational study. Patients were consecutively enrolled in a structured management program at a specialist centre for facial pain. Optimisation of medical treatment, physiotherapy, psychotherapy, and advice from trained nurses, were parts of the program. Medically intractable patients were referred for neurosurgery. Data-collection was prospective using standardised schemes and patient surveys. The aim was to describe the two-year outcome of medical treatment at the specialist centre. The primary outcome was a 50% reduction in the overall burden of pain according to a Numerical Rating Scale (NRS) after two years. RESULTS: A total of 186 primary TN patients were enrolled in the program of which 103 patients remained medically managed and completed the two-year follow-up. Fifty patients were treated surgically within the first two years of follow-up. Half of the medically managed patients (53 (51%)), had more than a 50% reduction in the overall burden of pain over the two-year period. The overall burden of pain on NRS decreased from mean 5.34 to 3.00, p < 0.01. There was no significant association between primary outcome and sex, depression and/or anxiety, concomitant persistent pain, or neurovascular contact with morphological changes of the trigeminal nerve. CONCLUSIONS: Patients with trigeminal neuralgia improve over a two-year period when enrolled in a structured medical management program. Optimisation of drug treatment, continuous advice and education and support by the multidisciplinary team, referral of the medically intractable patients for surgery or the natural history of the disease, can be some of the reasons for the improvement. The favourable prognosis provides hope and optimism for medically managed TN patients. TRIAL REGISTRATION: Current study was observational, and patients were offered standard clinical care and laboratory workups according to current American Academy of Neurology and European Federation of Neurological Societies treatment guidelines. The study has been registered at ClincalTrials.gov. ID: NCT03838393 .

The Effects of Naturalistic Light on Diurnal Plasma Melatonin and Serum Cortisol Levels in Stroke Patients during Admission for Rehabilitation: A Randomized Controlled Trial.

Background: Stroke patients admitted for rehabilitation often lack sufficient daytime blue light exposure due to the absence of natural light and are often exposed to light at unnatural time points. We hypothesized that artificial light imitating daylight, termed naturalistic light, would stabilize the circadian rhythm of plasma melatonin and serum cortisol levels among long-term hospitalized stroke patients. Methods: A quasi-randomized controlled trial. Stroke patients in need of rehabilitation were randomized between May 1, 2014, and June 1, 2015 to either a rehabilitation unit equipped entirely with always on naturalistic lighting (IU), or to a rehabilitation unit with standard indoor lighting (CU). At both inclusion and discharge after a hospital stay of at least 2 weeks, plasma melatonin and serum cortisol levels were measured every 4 hours over a 24-hour period. Circadian rhythm was estimated using cosinor analysis, and variance between time-points. Results: A total of 43 were able to participate in the blood collection. Normal diurnal rhythm of melatonin was disrupted at both inclusion and discharge. In the IU group, melatonin plasma levels were increased at discharge compared to inclusion (n = 23; median diff, 2.9; IQR: -1.0 to 9.9, p = 0.030) and rhythmicity evolved (n = 23; p = 0.007). In the CU group, melatonin plasma levels were similar between discharge and inclusion and no rhythmicity evolved. Overall, both patient groups showed normal cortisol diurnal rhythms at both inclusion and discharge. Conclusions: This study is the first to demonstrate elevated melatonin plasma levels and evolved rhythmicity due to stimulation with naturalistic light.

Prognostic factors for outcome of microvascular decompression in trigeminal neuralgia: A prospective systematic study using independent assessors.

INTRODUCTION: There is a lack of high-quality prospective, systematic studies using independent assessors of outcome of microvascular decompression as treatment for trigeminal neuralgia. METHODS: Clinical characteristics and outcome data were recorded prospectively from consecutive classical trigeminal neuralgia patients, using standardized interviews. Degree of neurovascular contact was evaluated by a 3.0 Tesla MRI blinded to symptomatic side. Patients were assessed before and 12 months after surgery by a neurologist. RESULTS: Twenty-six men and 33 women completed 12 months follow-up. Forty-one patients (69%) had an excellent outcome (no pain, no medication). Ten (18%) patients had a good outcome. Eight (12%) patients had no improvement or had worsening of pain. MRI showed neurovascular contact with morphological changes in 34 patients (58%). Odds ratio between neurovascular contact with morphological changes and excellent outcome was 4.4 (Cl 1.16-16.26), p = 0.029. Odds ratio between male sex and excellent outcome was 11.38 (Cl 2.12-59.52), p = 0.004. No significant association was found between excellent outcome and concomitant persistent pain, current age or disease duration. CONCLUSION: Neurovascular contact with morphological changes and male sex are positive predictive factors for outcome of microvascular decompression. The findings enable clinicians to better inform patients before surgery.

Altered thalamic connectivity during spontaneous attacks of migraine without aura: A resting-state fMRI study.

Background Functional connectivity of brain networks may be altered in migraine without aura patients. Functional magnetic resonance imaging (fMRI) studies have demonstrated changed activity in the thalamus, pons and cerebellum in migraineurs. Here, we investigated the thalamic, pontine and cerebellar network connectivity during spontaneous migraine attacks. Methods Seventeen patients with episodic migraine without aura underwent resting-state fMRI scan during and outside of a spontaneous migraine attack. Primary endpoint was a difference in functional connectivity between the attack and the headache-free days. Functional connectivity was assessed in four different networks using seed-based analysis. The chosen seeds were in the thalamus (MNI coordinates x,y,z: right, 22,-24,0 and left, -22,-28,6), pons (right, 8,-24,-32 and left, -8,-24,-32), cerebellum crus I (right, 46,-58,-30 and left, -46,-58,-30) and cerebellum lobule VI (right, 34,-42,-36 and left, -32,-42,-36). Results We found increased functional connectivity between the right thalamus and several contralateral brain regions (superior parietal lobule, insular cortex, primary motor cortex, supplementary motor area and orbitofrontal cortex). There was decreased functional connectivity between the right thalamus and three ipsilateral brain areas (primary somatosensory cortex and premotor cortex). We found no change in functional connectivity in the pontine or the cerebellar networks. Conclusions The study indicates that network connectivity between thalamus and pain modulating as well as pain encoding cortical areas are affected during spontaneous migraine attacks.

Increased brainstem perfusion, but no blood-brain barrier disruption, during attacks of migraine with aura.

See Moskowitz (doi:10.1093/brain/awx099) for a scientific commentary on this article.The migraine aura is characterized by transient focal cortical disturbances causing dramatic neurological symptoms that are usually followed by migraine headache. It is currently not understood how the aura symptoms are related to the headache phase of migraine. Animal studies suggest that cortical spreading depression, the likely mechanism of migraine aura, causes disruption of the blood-brain barrier and noxious stimulation of trigeminal afferents leading to activation of brainstem nuclei and triggering of migraine headache. We used the sensitive and validated technique of dynamic contrast-enhanced high-field magnetic resonance imaging to simultaneously investigate blood-brain barrier permeability and tissue perfusion in the brainstem (at the level of the lower pons), visual cortex, and brain areas of the anterior, middle and posterior circulation during spontaneous attacks of migraine with aura. Patients reported to our institution to undergo magnetic resonance imaging during the headache phase after presenting with typical visual aura. Nineteen patients were scanned during attacks and on an attack-free day. The mean time from attack onset to scanning was 7.6 h. We found increased brainstem perfusion bilaterally during migraine with aura attacks. Perfusion also increased in the visual cortex and posterior white matter following migraine aura. We found no increase in blood-brain barrier permeability in any of the investigated regions. There was no correlation between blood-brain barrier permeability, brain perfusion, and time from symptom onset to examination or pain intensity. Our findings demonstrate hyperperfusion in brainstem during the headache phase of migraine with aura, while the blood-brain barrier remains intact during attacks of migraine with aura. These data thus contradict the preclinical hypothesis of cortical spreading depression-induced blood-brain barrier disruption as a possible mechanism linking aura and headache.awx089media15422686892001.

Persistent idiopathic facial pain - a prospective systematic study of clinical characteristics and neuroanatomical findings at 3.0 Tesla MRI.

Introduction Persistent idiopathic facial pain (PIFP) is a poorly understood chronic orofacial pain disorder and a differential diagnosis to trigeminal neuralgia. To address the lack of systematic studies in PIFP we here report clinical characteristics and neuroimaging findings in PIFP. Methods Data collection was prospective and standardized in consecutive PIFP patients. All patients underwent 3.0 MRI. Results In a cohort of 53 PIFP patients, the average age of onset was 44.1 years. PIFP was found in more women 40 (75%) than men 13 (25%), p < 0.001. There was a high prevalence of bilateral pain 7 (13%), hypoesthesia 23 (48%), depression 16 (30%) and other chronic pain conditions 17 (32%) and a low prevalence of stabbing pain 21 (40%), touch-evoked pain 14 (26%) and remission periods 10 (19%). The odds ratio between neurovascular contact and the painful side was 1.4 (95% Cl 0.4-4.4, p = 0.565) and the odds ratio between neurovascular contact with displacement of the trigeminal nerve and the painful side was 0.2 (95% Cl 0.0-2.1, p = 0.195). Conclusion PIFP is separated from trigeminal neuralgia both with respect to the clinical characteristics and neuroimaging findings, as NVC was not associated to PIFP.

[Diagnostics and treatment of trigeminal neuralgia].

Trigeminal neuralgia (TN) is characterized by unilateral evoked short-lasting intense pain paroxysms in the face. A concomitant persistent background pain is frequently present. Neurovascular contact causing displacement or atrophy of the trigeminal nerve is important to TN aetiology. TN can also be secondary to a space-occupying lesion or multiple sclerosis. Early high-quality magnetic resonance imaging is mandatory as a part of the work-up. First-choice treatment is medical. Medically refractory patients are referred to neurosurgery. Nationwide in Denmark, there is a need for structured and uniform treatment of TN.

Quantitative sensory testing in classical trigeminal neuralgia-a blinded study in patients with and without concomitant persistent pain.

The diagnostic criteria of the third International Classification of Headache Disorders state that there should be no neurological deficits in patients with classical trigeminal neuralgia (TN) at clinical examination. However, studies demonstrating sensory abnormalities at bedside examination in TN patients have questioned this. Our aim was to examine whether TN patients without sensory abnormalities at neurological examination have sensory abnormalities at quantitative sensory testing (QST) and whether there were any QST differences between TN with and without concomitant persistent pain. Thirty-six TN patients were investigated with the standardized QST protocol by the German Research Network on Neuropathic Pain. The investigators were blinded to presence of concomitant persistent pain and symptomatic side. Based on comparison to the German Research Network on Neuropathic Pain controls, z scores were calculated to process frequency analyses and Z-profiles. We found increased mechanical detection threshold on the symptomatic side (47.2% vs 0%, P = 0.008), asymptomatic side (33.3% vs 0%, P = 0.011), and hand (36% vs 0%, P < 0.001) in TN compared with controls. The Z-profiles demonstrated increased mechanical detection threshold on the symptomatic side compared with the asymptomatic side (-2.980 vs -2.166, P = 0.040). Thermal and mechanical hyperalgesia was detected bilaterally in the face and the hand. Trigeminal neuralgia patients with concomitant persistent pain tended to have higher mean z score values compared to TN with purely paroxysmal pain indicative of decreased detection thresholds. Trigeminal neuralgia patients with no sensory abnormalities at neurological examination had generalized subclinical hypoesthesia, which was more pronounced on the symptomatic side, and thermal and mechanical hyperalgesia. This could indicate pain-induced hypoesthesia and sensitization induced by central mechanisms.

Migraine induced by hypoxia: an MRI spectroscopy and angiography study.

Migraine with aura is prevalent in high-altitude populations suggesting an association between migraine aura and hypoxia. We investigated whether experimental hypoxia triggers migraine and aura attacks in patients suffering from migraine with aura. We also investigated the metabolic and vascular response to hypoxia. In a randomized double-blind crossover study design, 15 migraine with aura patients were exposed to 180 min of normobaric hypoxia (capillary oxygen saturation 70-75%) or sham on two separate days and 14 healthy controls were exposed to hypoxia. Glutamate and lactate concentrations in the visual cortex were measured by proton magnetic resonance spectroscopy. The circumference of cranial arteries was measured by 3 T high-resolution magnetic resonance angiography. Hypoxia induced migraine-like attacks in eight patients compared to one patient after sham (P = 0.039), aura in three and possible aura in 4 of 15 patients. Hypoxia did not change glutamate concentration in the visual cortex compared to sham, but increased lactate concentration (P = 0.028) and circumference of the cranial arteries (P < 0.05). We found no difference in the metabolic or vascular responses to hypoxia between migraine patients and controls. In conclusion, hypoxia induced migraine-like attacks with and without aura and dilated the cranial arteries in patients with migraine with aura. Hypoxia-induced attacks were not associated with altered concentration of glutamate or other metabolites. The present study suggests that hypoxia may provoke migraine headache and aura symptoms in some patients. The mechanisms behind the migraine-inducing effect of hypoxia should be further investigated.

Trigeminal neuralgia--a coherent cross-specialty management program.

BACKGROUND: Optimal management of patients with classical trigeminal neuralgia (TN) requires specific treatment programs and close collaboration between medical, radiological and surgical specialties. Organization of such treatment programs has never been described before. With this paper we aim to describe the implementation and feasibility of an accelerated cross-speciality management program, to describe the collaboration between the involved specialties and to report the patient flow during the first 2 years after implementation. Finally, we aim to stimulate discussions about optimal management of TN. METHODS: Based on collaboration between neurologists, neuroradiologists and neurosurgeons a standardized program for TN was implemented in May 2012 at the Danish Headache Center (DHC). First out-patient visit and subsequent 3.0 Tesla MRI scan was booked in an accelerated manner. The MRI scan was performed according to a special TN protocol developed for this program. Patients initially referred to neurosurgery were re-directed to DHC for pre-surgical evaluation of diagnosis and optimization of medical treatment. Follow-up was 2 years with fixed visits where medical treatment and indication for neurosurgery was continuously evaluated. Scientific data was collected in a structured and prospective manner. RESULTS: From May 2012 to April 2014, 130 patients entered the accelerated program. Waiting time for the first out-patient visit was 42 days. Ninety-four percent of the patients had a MRI performed according to the special protocol after a mean of 37 days. Within 2 years follow-up 35% of the patients were referred to neurosurgery after a median time of 65 days. Five scientific papers describing demographics, clinical characteristics and neuroanatomical abnormalities were published. CONCLUSION: The described cross-speciality management program proved to be feasible and to have acceptable waiting times for referral and highly specialized work-up of TN patients in a public tertiary referral centre for headache and facial pain. Early high quality MRI ensured correct diagnosis and that the neurosurgeons had a standardized basis before decision-making on impending surgery. The program ensured that referral of the subgroup of patients in need for surgery was standardized, ensured continuous evaluation of the need for adjustments in pharmacological management and formed the basis for scientific research.

Association between neurovascular contact and clinical characteristics in classical trigeminal neuralgia: A prospective clinical study using 3.0 Tesla MRI.

BACKGROUND: Previous studies demonstrated that a severe neurovascular contact (NVC) causing displacement or atrophy of the trigeminal nerve is highly associated with classical trigeminal neuralgia (TN). There are no studies describing the association between the clinical characteristics of TN and severe NVC. METHODS: Clinical characteristics were prospectively collected from consecutive TN patients using semi-structured interviews in a cross-sectional study design. We evaluated 3.0 Tesla MRI blinded to the symptomatic side. RESULTS: We included 135 TN patients. Severe NVC was more prevalent in men (75%) compared to women (38%) (p < 0.001), and the odds in favor of severe NVC on the symptomatic side were 5.1 times higher in men compared to women (95% CI 2.3-10.9, p < 0.001). There was no difference between patients with and without severe NVC in age (≥60 years vs. <60) (OR 1.6 95% CI (0.8-3.4), p = 0.199) or duration of disease (p = 0.101). CONCLUSIONS: Severe NVC was much more prevalent in men than in women, who may more often have other disease etiologies causing or contributing to TN. Severe NVC was not associated with age or with duration of disease.

Significance of neurovascular contact in classical trigeminal neuralgia.

Neurovascular contact is considered a frequent cause of classical trigeminal neuralgia and microvascular decompression with transposition of a blood vessel is preferred over other surgical options in medically refractory patients with classical trigeminal neuralgia. However, the prevalence of neurovascular contact has not been investigated in a representative cohort of patients with classical trigeminal neuralgia based in a neurological setting and using high-quality neuroimaging and blinded evaluation. We aimed to investigate whether presence and degree of neurovascular contact are correlated to pain side in classical trigeminal neuralgia. Consecutive classical trigeminal neuralgia patients with unilateral symptoms were referred to 3.0 T magnetic resonance imaging and included in a cross-sectional study. Magnetic resonance imaging scans were evaluated blindly and graded according to presence and degree of neurovascular contact. Severe neurovascular contact was defined as displacement or atrophy of the trigeminal nerve. A total of 135 patients with classical trigeminal neuralgia were included. Average age of disease onset was 53.0 years (95% confidence interval mean 40.5-55.5) and current age was 60.1 years (95% % confidence interval mean 57.5-62.7). Eighty-two (61%, 95% confidence interval 52-69%) patients were female. Neurovascular contact was prevalent both on the symptomatic and asymptomatic side [89% versus 78%, P = 0.014, odds ratio = 2.4 (1.2-4.8), P = 0.017], while severe neurovascular contact was highly prevalent on the symptomatic compared to the asymptomatic side [53% versus 13%, P < 0.001, odds ratio = 11.6 (4.7-28.9), P < 0.001]. Severe neurovascular contact was caused by arteries in 98%. We conclude that neurovascular contact causing displacement or atrophy of the trigeminal nerve is highly associated with the symptomatic side in classical trigeminal neuralgia as opposed to neurovascular contact in general. Our findings demonstrate that severe neurovascular contact is involved in the aetiology of classical trigeminal neuralgia and that it is caused by arteries located in the root entry zone.