Headache is one of the most common presentations in neurology accounting for 1 in 3 neurology referrals [1]. Among the primary causes, migraine is the second most common form of headache and holds the eighth rank among the top 20 causes of the disease burden as per the disability-adjusted life years (DALY) criteria [2]. Its prevalence in India was estimated to be approximately 14.12% with a maximum burden among women aged between 30 and 34 years. [3] Idiopathic intracranial hypertension (IIH) is a relatively uncommon headache disorder due to raised intracranial pressure usually seen in obese people with a risk of loss of vision in one or both eyes if untreated [4]. The worldwide incidence of IIH is around 0.5–2 per 100,000 people per year [5]. Reported female-to-male ratio in IIH range from 4:1–15:1 [6].

Pathophysiology of these diverse headache types is dependent on complex hemodynamic mechanisms as evident in migraine [7]. In the landmark paper Olesen described focal oligemia in the occipitoparietal region in the prodromal phase which gradually spread anteriorly over the next 15–45 minutes with concomitant headache. The regional cerebral blood flow was impaired in all patients with activity [8]. However, the main pathophysiological basis proposed for IIH has been the CSF outflow dynamics [9]. Recently, chronic inflammation secondary to dysregulated cortisol secretion in the body has been proposed as a pathogenetic process [10]. Cerebral blood flow has been found to have a link with IIH by inducing cerebral hyperemia thereby having a quadratic correlation coefficient with the venous pressure [11]. Hence, these studies prove the complex interplay of cerebral blood flow, intracranial pressure, and CSF dynamics in both types of headaches.

ICP measurement is usually done by a lumbar puncture to diagnose IIH and may be needed to diagnose headaches of other causes. Diagnosis of migraine is clinical. However, upto 63% of patients of IIH were shown to have headaches that fulfilled the ICHD-2 criteria for migraine. [12] In a separate study, out of 44 patients of chronic unresponsive migraine with evidence of sinus stenosis in magnetic resonance venography, 38 (86.4%) had opening CSF pressures greater than 200 mm water and 70.5% satisfied the ICHD-II criteria for headache attributed to intracranial hypertension [13]. It is not known what additional factors apart from raised intracranial pressure distinguish IIH from other varieties of headaches.

Changes in intracranial flow velocities have been closely associated with the pathogenesis of headaches [14]. Transcranial Doppler (TCD) is an attractive and non-invasive alternative to invasive intracerebral monitoring methods with an overall accuracy ranging around ±12 mmHg, for dynamic changes of ICP in time, particularly when it is linked to a vascular with a great potential of tracing dynamical changes of ICP in time, particularly those of vasogenic nature [15], [16]. Vasomotor motor response (VMR), which can be easily measured by the breath-holding technique (BHT) in TCD is a robust indicator of cerebral autoregulation [17]. Increased ICP has been postulated to cause a decrease in VMR [18]. Under this premise using TCD, may prove to be useful to evaluate vessel wall function in a dynamic real-time scenario, in a non-invasive manner [19]. It works by the principle of vessel wall dilatation in response to increased carbon dioxide (CO2) levels causing increased flow velocities on TCD [20]. Intracranial flow velocities in migraine are increased as compared to normal healthy population suggesting a role of sterile neurogenic inflammation in migraine [21], [22]. Vasomotor reactivity to stress in migraine is variable with BHI ranging from 1.11 to 1.30 [23]. It has not been researched well for patients of IIH. The breath-holding index (BHI) represents a simple Doppler-based method to measure cerebral vasomotor response as described by Markus et al. [24] Literature is also limited in exploring the differences between these two headache types.

Most studies using vasoconstrictor stimuli demonstrated an increased vasomotor response in migraine subjects although some studies reported such an increase only in migraine with aura [25]. There is not much literature to study the differences or variations in intracranial flow velocities in IIH and migraine. The purpose of our study is to determine and compare VMR using TCD in patients of IIH, migraine, and normal population as an attempt to understand the role of intracranial hemodynamics in the pathogenesis of both disease states and normal intracerebral vasculature.