In the latest Case Record of the Massachusetts General Hospital, a 69-year-old man was admitted to this hospital because of dizziness and vomiting, which had begun abruptly 9 hours earlier, on awakening. Examination revealed nystagmus and a wide-based gait. CT revealed no intracranial hemorrhage. A diagnostic procedure was performed.
Stroke is the leading cause of serious long-term disability in the U.S; it kills one American every 4 minutes.
• How can central and peripheral causes of vertigo be distinguished?
While peripheral vertigo is more prevalent than central vertigo in the general population, in patients with vascular risk factors, peripheral vertigo should be a diagnosis of exclusion. The consequences of vertebrobasilar stroke are too devastating to be missed, with up to 50% mortality. Central vertigo is associated with lesions in the posterior fossa, such as the cerebellum. Nystagmus in central vertigo is typically horizontal, vertical, or rotatory (toward the side of the lesion), whereas peripheral nystagmus is often horizontal or rotatory, but can be variable. Response to provocative maneuvers such as Baranay’s has a short latency in central vertigo and a longer latency (up to 20 seconds) in peripheral etiologies. Nausea or vomiting can occur in both central and peripheral injury, but is often more severe in onset in peripheral causes. A central etiology is often accompanied by a headache. Gait ataxia is seen in a central origin due to cerebellar lesions, and the presence of cranial nerve findings helps to localize the lesion to the level of injury in the posterior fossa. Peripheral vertigo tends to be more position dependent than central vertigo.
• How are hemorrhagic strokes classified?
Currently, hemorrhagic strokes are roughly classified with respect to location — subarachnoid, epidural, subdural, or intraparenchymal. Subarachnoid hemorrhage is typically characterized by an early severe headache and progression to global alteration in consciousness. Epidural hemorrhage, commonly from traumatic injury of the middle meningeal artery, occurs in a younger age group, when the potential space between the skull and the dura are easier to separate. In this patient’s age group, especially after trauma, subdural hemorrhage can be associated with focal progressive neurologic changes, and a chronic subdural can cause seizures or re-expand in the setting of anticoagulants. More recently recognized causes of intraparenchymal hemorrhage, such as cerebral amyloid angiopathy, may have a more indolent course and may result in cognitive changes. The cerebellum and basal ganglia are common locations of intraparenchymal hemorrhage from hypertension.
Morning Report Questions
Q: What are the subtypes of ischemic stroke and their associated risk factors?
A: Venous strokes due to cerebral venous thromboses are less common than arterial ischemic strokes, developing over days or weeks, and are frequently missed. Venous hypercoagulability, worsening headache, visual acuity changes, papilledema, or the late development of a hemorrhagic lesion (due to venous congestion) should prompt an urgent workup for cerebral venous thrombosis. Arterial strokes, the majority of ischemic infarcts, comprise thrombotic (large vessel or small vessel), embolic (cardioembolic or paradoxical embolic), and other vasospastic variants. A large proportion (>30%) are cardioembolic, at all ages. Traditionally, age, gender, and race all contribute to the distribution of stroke subtypes — older age with higher proportion of large-vessel atherosclerotic disease, cognitive impairment with small-vessel disease, and younger age with traumatic dissection and congenital disease. Important new causes of stroke are discovered in the “cryptogenic” category — stroke of unclear cause after a standard workup, including genetic variants, such as CADASIL, subclinical paroxysmal atrial fibrillation undetected by short-term cardiac monitoring, or cardiac abnormalities, such as patent foramen ovale (PFO). PFO is associated with over 40% of cryptogenic strokes.
Q: How is a stroke secondary to arterial dissection managed?
A: Acute ischemic stroke related to arterial dissection is often treated with thrombolysis. Thrombolysis with IV tissue plasminogen activator (tPA) is the first-line treatment for acute ischemic stroke, typically within three hours of symptom onset. Major clinical trials did not exclude cases of dissection, and meta-analysis demonstrated no difference in the risk of hemorrhage in patients with dissection.
Treatment for dissection outside of the acute setting needs to be individualized, since there are no large trials to support anticoagulation or antiplatelet therapy. While it seems risky and counterintuitive to anticoagulate a torn blood vessel, cerebrovascular dissections are rarely actual ruptures of the vessel, but rather separations of the intima from the rest of the vascular wall; the prothrombotic intimal flap can act as source of distal emboli. Dissection can rarely occur within the tunica media or adventitia, resulting in pseudoaneurysm or vessel-wall rupture and subarachnoid hemorrhage. This is more common in posterior circulation intracranial dissection and spontaneous dissections associated with collagen vascular disease (e.g., Marfan’s syndrome and fibromuscular dysplasia). Overall clinical experience indicates that the risk of hemorrhage is relatively low for intracranial dissection. Unless there is evidence of subarachnoid hemorrhage or extensive intracranial vertebral-artery dissection with the formation of a pseudoaneurysm, careful anticoagulation therapy for 3 to 6 months, to give injured vessels a chance to recanalize, can maximize the risk-benefit ratio, because the chance of emboli is highest within the first few months.