ANTERIOR CEREBRAL ARTERY INFARCTION
Occlusion of the anterior cerebral artery is uncommon (0.5% to 3% of all strokes25), but when unilateral occlusion occurs, it can cause contralateral sensory and motor symptoms in the lower extremity, with sparing of the hands and face. In addition, a left-sided lesion is typically associated with akinetic mutism and transcortical motor aphasia (repetition ability retained), whereas right-sided infarction can result in confusion and motor hemineglect. Bilateral occlusion can cause a combination of the above symptoms, but was particularly associated with mutism, incontinence, and poor outcome in one small series.26
MIDDLE CEREBRAL ARTERY INFARCTION
The middle cerebral artery is the vessel most commonly involved in stroke, and clinical findings can be quite variable, depending on exactly where the lesion is located and which brain hemisphere is dominant. (In right-handed patients and in up to 80% of left-handed patients, the left hemisphere is dominant.) A middle cerebral artery stroke typically presents with hemiparesis, facial plegia, and sensory loss contralateral to the affected cortex. These deficits variably affect the face and upper extremity more than the lower extremity. If the dominant hemisphere is involved, aphasia (receptive, expressive, or both) is often present. If the nondominant hemisphere is involved, inattention, neglect, extinction on double-simultaneous stimulation, dysarthria without aphasia, and constructional apraxia (difficulty in drawing complex two-dimensional or three-dimensional figures) may occur. A homonymous hemianopsia and gaze preference toward the side of the infarct may also be seen, regardless of the side of the infarction.
POSTERIOR CEREBRAL ARTERY INFARCTION (DISTAL POSTERIOR CIRCULATION)
The classic symptoms and signs of posterior circulation strokes include ataxia, nystagmus, altered mental status, and vertigo, but presentation can sometimes be rather subtle.27 Crossed neurologic deficits (e.g., ipsilateral cranial nerve deficits with contralateral motor weakness) may indicate a brainstem lesion. According to an analysis of a large stroke registry,28 symptoms of posterior cerebral artery involvement include unilateral limb weakness, dizziness, blurry vision, headache, and dysarthria. Common presenting signs include visual field loss, unilateral limb weakness, gait ataxia, unilateral limb ataxia, cranial nerve VII signs, lethargy, and sensory deficits.28 Visual field loss, classically described as contralateral homonymous hemianopsia and unilateral cortical blindness, is thought to be specific for distal posterior circulation stroke because the visual centers of the brain are supplied by the posterior cerebral artery. Light-touch and pinprick sensation deficits, loss of ability to read (alexia) without agraphia, inability to name colors, recent memory loss, unilateral third nerve palsy, and hemiballismus have also been reported. Motor dysfunction, although common, is typically minimal, which can keep some patients from realizing they have had a stroke.
BASILAR ARTERY OCCLUSION (MIDDLE POSTERIOR CIRCULATION)
Occlusion of the basilar artery most commonly presents with symptoms of unilateral limb weakness, dizziness, dysarthria, diplopia, and headache.28 The most common presenting signs are unilateral limb weakness, cranial nerve VII signs, dysarthria, Babinski sign, and oculomotor signs.28 Dysphagia, nausea or vomiting, dizziness, and Horner's syndrome are positively correlated with basilar artery occlusion.28 Basilar artery occlusion can also rarely cause locked-in syndrome, which occurs with bilateral pyramidal tract lesions in the ventral pons and is characterized by complete muscle paralysis except for upward gaze and blinking. Basilar artery occlusions have a high risk of death and poor outcomes.29
VERTEBROBASILAR INFARCTION (PROXIMAL POSTERIOR CIRCULATION)
Patients with vertebrobasilar infarction most commonly present with symptoms of dizziness, nausea or vomiting, headache, dysphagia, unilateral limb weakness, and unilateral cranial nerve V symptoms.28 Common presenting signs include unilateral limb ataxia, nystagmus, gait ataxia, cranial nerve V signs, limb sensory deficit, and Horner's syndrome.28 For further discussion of vertigo, see chapter 170, "Vertigo."
Patients with cerebellar infarction can present with very nonspecific symptoms and frequently present with dizziness (with or without vertigo), nausea and vomiting, gait instability, headache, limb ataxia, dysarthria, nystagmus, and cranial nerve abnormalities.30 Mental status may vary from alert to comatose. Because CT is inadequately sensitive for posterior fossa lesions, obtain a diffusion-weighted MRI (DWI-MRI) when this diagnosis is suspected. A CT angiogram or magnetic resonance angiogram is useful to characterize any vascular lesion once the diagnosis is made. The clinical presentation and course of cerebellar infarction can be frustratingly difficult to predict, but the clinician must remain vigilant to the possibility of rapid deterioration secondary to increased brainstem pressure caused by cerebellar edema. Therefore, extremely close serial examinations (especially looking for gaze palsy and altered mental status) and prompt neurologic and neurosurgical bedside consultations are needed. Obtain early neurosurgical consultation for patients with cerebellar infarction. Cerebellar edema can lead to rapid deterioration with herniation, and consultation is required to determine the need for emergency posterior fossa decompression in these patients. Acute obstructing hydrocephalus requires treatment of elevated intracranial pressure and emergent surgical decompression.30
Lacunar infarcts are pure motor or sensory deficits caused by infarction of small penetrating arteries and are commonly associated with chronic hypertension and increasing age. The presentation is variable based on the location and size of the lesions. The prognosis is generally considered more favorable than for other stroke syndromes.
CAROTID AND VERTEBRAL ARTERY DISSECTION
Carotid or vertebral artery dissection is an uncommon but important cause of stroke (10% to 25% of cases), especially in young and middle-aged patients.31 A history of neck trauma in the days to weeks prior to presentation is a prominent risk factor. The trauma is usually minor32 (e.g., manipulative therapy of the neck33 or sport-related trauma34). Other risk factors include connective tissue disease,35 history of migraine,36 large vessel arteriopathies,37 and hypertension.38
The typical first symptom of patients with carotid or vertebral artery dissection is unilateral headache (68%), neck pain (39%), or face pain (10%),39-41 which can precede other symptoms by hours to days (median, 4 days).42 New-onset headache or neck pain of unclear etiology is such an important symptom that imaging of the neck vessels is recommended by some as part of initial evaluation.41 Symptoms may be transient or persistent. The median time between an initial presentation of neck pain and the development of other neurologic symptoms is 14 days, but if headache is the first symptom, other neurologic symptoms follow within a median time of 15 hours.42
Carotid Artery Dissection
The headache is most commonly in the frontotemporal region and, due to its variable quality and severity, may mimic subarachnoid hemorrhage (i.e., "thunderclap" headache), temporal arteritis, or preexisting migraine. A partial Horner's syndrome (miosis and ptosis) has traditionally been linked to carotid artery dissection, but in reality, it occurs in only about 25% of patients and is a sign accompanying other disorders besides stroke.43 Associated cranial nerve palsies have been reported in 12% of carotid artery dissections.44 Carotid dissection can progress to cause cerebral ischemia or, rarely, retinal infarction.
Vertebral Artery Dissection
Vertebral artery dissection commonly presents with neck pain (66%) and headache (65%), both of which can be unilateral or bilateral.40 The headache is typically occipital, but can rarely present with pain on an entire side of the head or in the frontal region.39 Other symptoms and signs may include unilateral facial paresthesia, dizziness, vertigo, nausea/emesis, diplopia and other visual disturbances, ataxia, limb weakness, numbness, dysarthria, and hearing loss. Cervical radiculopathy (typically a peripheral motor deficit at the C5 level) is a rare presentation (1%) and can also involve multiple levels and sensory findings.45 Untreated vertebral artery dissection may result in infarction in regions of the brain supplied by the posterior circulation.
MRI/magnetic resonance angiography and CT/CT angiography are the diagnostic modalities of choice for suspected carotid, vertebral, or basilar artery dissection.46 Choice of study is usually determined by consultation with the neurologist and radiologist.47 Color duplex US may not detect important vascular lesions.48,49
Treatment of Carotid and Vertebral Artery Dissection
In the absence of contraindications, carotid and vertebral artery dissection has been traditionally treated with IV heparin followed by warfarin (to maintain an INR of 2.0 to 3.0). This treatment has persisted despite the absence to date of published, high-quality randomized controlled trials comparing anticoagulation with other potentially more effective treatment modalities.50 In 2012, the nonrandomized arm (88 patients) of the Cervical Artery Dissection in Stroke Study was published along with a meta-analysis of previous trials.51 These preliminary results showed no difference between anticoagulation and antiplatelet therapy in terms of prevention of stroke after cervical artery dissection. Nonrandomized data regarding endovascular approaches to cervical artery dissection have been published, but no randomized controlled trial has been published yet. Therefore, pending the availability of new randomized controlled trial data, administer either anticoagulant or antiplatelet therapy in the ED in conjunction with appropriate specialist consultation.