Diffuse cerebral fat embolism is related to severe bone trauma. As a rule, the emboli are minute and widely dispersed, giving rise first to pulmonary symptoms and then to multiple dermal (anterior axillary fold and elsewhere) and cerebral petechial hemorrhages. Accordingly, the clinical picture is more of an encephalopathy and not strictly focal as it is in a stroke, although in some instances there may be focal features. Cerebral air embolism is a rare complication of abortion, scuba diving, or cranial, cervical, or thoracic operations involving large venous structures or venous catheter insertion; it was formerly encountered as a complication of pneumothorax therapy. Clinically, cerebral air embolism may be difficult to separate from the deficits following hypotension or hypoxia with which it frequently coexists. Hyperbaric treatment may be effective if instituted early.
Despite the large number of established sources of emboli, the point of origin cannot be determined in 20 to 30 percent or more of presumed embolic strokes. In such cases, emboli likely have originated from thrombi in the cardiac chambers or an occult arrhythmia but have left behind no residual clot and may be undetectable even by sophisticated methods, such as transesophageal echocardiography and newer MR techniques. Other cases may be a result of atheromatous material arising from the aorta or paradoxical embolism. If extensive evaluation fails to disclose the origin, the odds still favor a source in the left heart. Often, the diagnosis of cerebral embolism is made at autopsy without finding a source. In these cases, one presumes that the search for a thrombotic nidus may not have been sufficiently thorough and small thrombi in the atrial appendage, endocardium (between the papillary muscles of the heart), the aorta and its branches, or pulmonary veins may have been overlooked. Nevertheless, the source of embolic material is not revealed in a number of cases.
Atherosclerosis is the usual underlying pathology for local vascular thrombosis. The evolution of clinical phenomena in cerebral thrombosis, both of large intracranial (basilar, carotid) or extracranial (carotid, vertebral) and small vessels (lacunes), is more variable than that of embolism and hemorrhage. In many cases, a thrombus is the final event in the occlusion of a vessel but the stroke that results can be from reduced blood flow through the stenotic or occluded vessel or by a mechanism of embolization from the thrombus to a distal territory. Small and large vessel occlusion can even coincide in that atherosclerosis in a large parent vessel occludes the orifice of a smaller tributary vessel.
In some patients with atherothrombosis the stroke is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction, TIAs, discussed further on. These transient prodromal episodes may herald the oncoming vascular event caused by atherothrombotic stroke. Occasionally embolism is preceded by a transient neurologic disorder but TIAs are generally considered as more closely aligned with atherothrombotic stroke. Nevertheless, it has become appreciated that an embolic stroke may give rise to a transitory neurologic syndrome but it remains the case that repetitive stereotyped TIAs usually signal atherothrombotic vascular disease.