Cerebral Venous and Sinus Thrombosis Neupsy Key anoxic brain injury symptoms

CVT has been attributed to numerous causes, yet even after extensive workup, almost 30% of CVT diagnoses remain idiopathic. ISCVT found that thrombophilia (34.1%) and oral contraception (54%, overall data corrected for females of childbearing age) accounted for a significant portion of the causes of CVT. Other important causes of CVT were puerperium (14%, overall data corrected for females of childbearing age) and pregnancy (6%, overall data corrected for females of childbearing age). Additionally, infection (especially of the ear, sinus, mouth, face, and neck) contributed to 12% of CVT cases in their data set, and malignancy (within and outside of the central nervous system [CNS], both solid tumor and hematologic) was found to have caused 7% of CVT in the ISCVT population.Anoxic brain injury symptoms


regarding genetic causes, marjot et al. Performed a meta-analysis of 26 studies: this included 1,183 CVT patients, explored six genes, and demonstrated a statistically significant association between CVT and two genes: factor V leiden (OR = 2.40; 95% CI, 1.75 to 3.30; P .00001) and prothrombin gene mutation (OR = 5.48; 95% CI, 3.88 to 7.74; P .00001). Finally, more than 44% of subjects were found to have more than one cause of CVT, an important fact to remember when exploring causes of CVT in hopes of preventing reoccurrence. Table 40.1 summarizes common causes of CVT.

When CVT does cause an increase in ICP, patients commonly present with the following neurologic signs: papilledema, diplopia (most commonly due to sixth nerve palsy), headache which worsens with recumbency, nausea/vomiting, and encephalopathy.Anoxic brain injury symptoms in addition to signs of increased ICP, focal neurologic deficits following cerebral ischemia or hemorrhage are also important clinical presentations in patients with CVT. The actual signs of the focal brain injury are attributed to the site of venous ischemia and are therefore variable but include focal weakness, sensory changes, visual field deficits, and aphasias. Further confounding this picture in CVT, the superior sagittal sinus, the most commonly involved cerebral venous structure in CVT, drains both cerebral hemispheres and therefore when thrombosed can cause bilateral deficits complicating neurologic localization. A small yet clinically important subset of CVT patients are those with deep CVT.Anoxic brain injury symptoms CVT affecting the basal ganglia or thalamus is commonly bilateral and can lead to venous ischemia or hemorrhages. CVT affecting the deep parts of the brain tend to be more severe and quickly results in profound deficits including altered mental status and coma.

TABLE 40.1 common causes of cerebral sinus thrombosis

Drugs

Oral contraceptives (especially in combination with tobacco and/or prothrombotic disease), hormone replacement therapy, asparaginase chemotherapy, tamoxifen, steroids, androgens

Hematologic diseases

Polycythemia, thrombocythemia, paroxysmal nocturnal hemoglobinuria

Hypercoagulable state

Protein C, S, or antithrombin III deficiency; factor V leiden mutation; prothrombin gene mutation; antiphospholipid syndrome (lupus anticoagulant/anticardiolipin antibody); nephrotic syndrome; hyperhomocysteinemia

anoxic brain injury symptoms

Infections

Encephalitis; cerebritis; meningitis; mastoiditis; otitis; sinusitis; infections of the mouth, face, and neck

Inflammatory diseases

Vasculitis, lupus, wegener granulomatosis, inflammatory bowel disease, behçet disease, thromboangiitis obliterans, sarcoidosis

Malignancy

CNS tumors with invasion of the venous sinus, hematologic cancers, hypercoagulable state due to malignancy

Obstetric

Pregnancy and puerperium

Trauma (including iatrogenic)

Head injury, lumbar puncture, neurosurgical procedures

CNS, central nervous system.

Adapted from frontera J, ed . Decision making in neurocritical care. New york: thieme; 2009.

The cavernous sinuses are a unique set of cerebral sinuses. They are deep bilateral structures at the base of the cerebrum that house the internal carotid artery, ophthalmic vein, branches of the sphenoid and superficial middle cerebral veins, as well as cranial nerves III, IV, V1, V2, and VI.Anoxic brain injury symptoms venous thrombosis affecting the cavernous sinuses are associated with palsies affecting these cranial nerves as well as pain, ptosis, chemosis, and proptosis. Increased intraocular pressure due to poor venous drainage can lead to loss of visual acuity. Most cavernous sinus thromboses are related to infection, typically due to staphylococcus aureus, although streptococcus pneumoniae, gram-negative rods, anaerobes, and occasionally fungal infections may be culprits. Spread of symptoms to the contralateral eye via the intracavernous sinuses may occur within 24 to 48 hours of the initial presentation and is pathognomonic for cavernous sinus thrombosis. Table 40.2 summarizes common syndromes associated with CVT.Anoxic brain injury symptoms