In lateral (transverse) sinus thrombophlebitis, which usually follows chronic infection of the middle ear, mastoid, or petrous bone, earache and mastoid tenderness are succeeded, after a period of a few days to weeks by generalized headache and in some instances, papilledema. If the thrombophlebitis remains confined to the transverse sinus, there are no other neurologic signs. Spread to the jugular bulb may give rise to the syndrome of the jugular foramen (see Table 44-1) and involvement of the torcula, leading to increased intracranial pressure. One lateral sinus, usually the right, is normally larger than the other, which may account for greatly elevated pressure when it is occluded. However, contiguous involvement of the superior sagittal sinus and cortical veins emanating from it causes seizures and focal cerebral signs (see in the following text).
Fever, as in all forms of septic intracranial thrombophlebitis tends to be present but intermittent, and other signs of the septic state may be prominent. The CSF has increased pressure but the formula is usually normal but may show a small number of cells and a modest elevation of protein content. The term “otitic hydrocephalus” was introduced for this condition by Sir Charles Symonds, giving the erroneous impression that hydrocephalus was the cause of raised intracranial pressure. It is mentioned here because his clinical description, as for many other conditions, remains an outstanding source.
Imaging by MR and CT are the main means of confirming the diagnosis of venous sinus thrombosis. MRI or CT are also able to detect the local source of infection in the bone or soft tissue and other secondary changes such as venous infarction, cerebral edema, abscess, and hydrocephalus. The distinction between septic and sterile venous sinus thrombosis is difficult to make unless there is adjacent infection. Certain characteristics such as intense contrast enhancement are suggestive of infection.
Prolonged administration of high doses of antibiotics is the mainstay of treatment. Anticoagulation, shown to be beneficial in small series of aseptic venous occlusion, is of uncertain value, but it is usually administered as well.
This condition is usually secondary to infections of the ethmoid, sphenoid, or maxillary sinuses or the skin around the eyes and nose, sometimes originating in a seemingly innocuous lesion. In addition to headache, high fluctuating fever, and signs of systemic toxicity, there are characteristic local effects. Obstruction of the ophthalmic veins leads to chemosis, proptosis, and edema of the ipsilateral eyelids, forehead, and nose. The retinal veins become engorged, which may be followed by retinal hemorrhages and papilledema. More often, however, vision in the affected eye is lost by a retrobulbar optic neuropathy as noted below, without visible alterations in the fundus. Involvement of the third, fourth, sixth, and ophthalmic and maxillary divisions of the fifth cranial nerves, which lie in the lateral wall of the cavernous sinus (see Chap. 33), leads to ptosis, varying degrees of ocular palsy, pain around the eye, and sensory loss over the maxilla and forehead. Within a few days, spread through the circular sinus to the opposite cavernous sinus results in bilateral symptoms. The posterior part of the cavernous sinus may become infected via the superior and inferior petrosal veins without the occurrence of orbital edema or ophthalmoplegia but usually with abducens and facial paralysis. The CSF is usually normal unless there is an associated meningitis or subdural empyema.