The eye will be positioned down and out due to unopposed innervation of the fourth and sixth cranial nerves.Other symptoms include severe headache; weakness of the extremities on the opposite side from the lesion due to compression of the crossed pyramid pathways; and vision loss, also on the opposite side, due to compression of the posterior cerebral artery. In rare cases, small hematomas may be asymptomatic.If not treated promptly, epidural hematomas can cause tonsillar herniation, resulting in respiratory arrest. The trigeminal nerve may be involved late in the process as the pons is compressed, but this is not an important presentation, because the person may already be dead by the time it occurs. In the case of epidural hematoma in the posterior cranial fossa, tonsillar herniation causes Cushings triad: hypertension, bradycardia, and irregular breathing. Causes
The most common cause of intracranial epidural hematoma is head injury, although spontaneous hemorrhages have been known to occur. Epidural hematomas occur in about 10% of traumatic brain injuries, mostly due to car accidents, assaults, or falls. They are often caused by acceleration-deceleration trauma and transverse forces.Epidural hematoma commonly results from a blow to the side (temporal bone) of the head. The pterion region, which overlies the middle meningeal artery, is relatively weak and prone to injury. Only 20 to 30% of epidural hematomas occur outside the region of the temporal bone. The brain may be injured by prominences on the inside of the skull as it scrapes past them.
Some have also recommended thrombolysis with catheter directed alteplase or mechanical thrombectomy with a large bore catheter and manual aspiration providing definitive intervention with an endovascular approach. If there is thoracic outlet syndrome or other anatomical cause then surgery can be considered to correct the underlying defect. History
The condition is named after two men. James Paget first proposed the idea of venous thrombosis causing upper extremity pain and swelling, and Leopold von Schrötter later linked the clinical syndrome to thrombosis of the axillary and subclavian veins. References


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