Thoracic outlet syndrome (TOS) is known to be associated with diffuse craniological comorbidities (CCM), such as occipital headaches, migraines, vestibular dysfunction, tinnitus and fatigue. Conventionally, these problems have been suggested to be a manifestation of positional vertebrobasilar insufficiency. Angiography tends to be normal in TOS sufferers, however, and doppler ultrasonography of the vertebral artery fails to demonstrate severe flow reduction. TOS is attributed to the brachial plexus and subclavian artery being compressed in the interscalene triangle, costoclavicular or subpectoral passages. The vertebral and carotid arteries arise from subclavian artery proximal to the sites of obstruction in TOS. Numerous reports of resolved CCM post-scalenectomy and first-rib resection, despite lacking vertebral artery impairment, have been documented. TOS CCM, moreover, share many of the symptoms seen in systemic and intracranial hypertension. Reports of subclavian thromboembolus migrating to the head have been documented in incidences of TOS, showing the potential for flow retrogradation. We postulate that the blood prevented from entering the brachium due to distal subclavian compression, retrogrades to the brain via the carotid and vertebral arteries, resulting in craniovascular hyperperfusion and congestion.  Abbreviations: Thoracic outlet syndrome: TOS, Vertebral artery: VA, Vertebrobasilar insufficiency: VBI, Cerebrovascular hyperperfusion: CVH, Blood-brain barrier: BBB, Myalgic encephalomyelitis: ME, “Time of flight”: TOF, Citation: Larsen K, Galluccio FC, Chand SK. Does thoracic outlet syndrome cause cerebrovascular hyperperfusion? Diagnostic markers for occult craniovascular congestion. Anaesth pain intensive care 2020;24(1)___ Received – 30 November 2019; Reviewed – 2, 6 February 2019; Accepted – 27 February 2019;