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Timothy C. Hain, MD
The purpose of this page is to consider the findings in brainstem strokes in detail. More general aspects of brainstem strokes and TIA's related to vertigo are considered elsewhere.
There are a large number of well described brainstem stroke syndromes. Most of these involve ischemia in the distribution of the basilar or vertebral arteries, as shown to the right. Here we will describe the most common syndromes. Clinically, in localizing strokes to the brainstem one looks for the "cardinal" feature of an ipsilateral peripheral cranial nerve involvement, and a contralateral weakness or sensory deficit. Cerebellar signs, if present, should be ipsilateral. MRI is frequently needed to make a specific diagnosis and to separate vascular etiologies from tumor and other structural injuries. The pattern of sensory disturbance may be helpful. A dissociated sensory deficit over the face or half the body usually indicates a lesion within the brainstem. A hemisensory loss involving all modalities indicates a lesion in the upper brainstem, in the thalamus, or deep in the white matter of the parietal lobe. Bilaterality of both motor and sensory signs is almost certain evidence of a brainstem lesion. When hemiplegia or hemiparesis and sensory loss are coextensive, the lesion usually lies supratentorially.
Vertigo is a common early symptom of brainstem strokes. However, because strokes are much less common than other sources of vertigo such as ear disorders, vertigo is only caused by central nervous system problems (including stroke) about 5% of the time. Migraine is a common cause of vascular vertigo.
Hearing disturbance is a much less common symptom of brainstem stroke than vertigo. This may reflect the resilience of the wiring pattern of hearing in the brainstem which includes of both crossed and uncrossed pathways, or factors related to details of the blood supply or resistance of the ear to disturbances in blood supply.
The PICA syndrome is also known as "lateral medullary syndrome", or "Wallenberg's syndrome", after Wallenberg's description in 1895. This is the most common brainstem stroke. It is typified by vertigo, ipsilateral hemiataxia, dysarthria, ptosis and miosis. Most patients with this stroke recover very well and often resume their previous activities (Nelles et al, 1998). Patients often have a Horner's syndrome (unilateral ptosis, miosis and facial anhidrosis). There also may be saccadic dysmetria (overshoot), saccadic pulsion (pulling of the eye during vertical saccades toward the side of lesion). Prognosis is generally quite good with full or near full recovery expected at 6 months. Diagnosis is generally via MRI. ABR testing is often abnormal in persons with central Horner's syndrome (Faught and Oh, 1985), but generally not abnormal in Wallenberg's as the site of lesion is below the auditory pathways.
PICA may arise from the vertebral artery, or as a separate branch of the basilar artery.
The AICA syndrome is usually accompanied by vertigo and unilateral ipsilateral deafness from labyrinthine artery ischemia, ipsilateral facial weakness and ataxia. It is the second most common brainstem stroke, about 10% of PICA frequency. The extent of this stroke is extremely variable. The AICA also has a very variable origin and may take origin from the caudal to middle pons. Diagnosis is generally via MRI.
The labyrinthine or internal auditory artery usually takes its origin from AICA, but it can also take origin from PICA or the basilar artery.It supplies the inner ear. In the internal auditory canal or IAC it supplies Scarpa's ganglion. After exiting it divides into the common cochlear artery and anterior vestibular artery. The common cochlear artery further divides into the main cochlear artery and the vestibulocochlear artery, the latter forming the posterior vestibular artery and the vestibular ramus. The main cochlear artery supplies the apical 3/4 of the cochlea, and the cochlear ramus, the basal 1/4 (high frequencies). The posterior vestibular artery supplies the inferior saccule and the ampulla of the posterior SCC. The anterior vestibular artery is a smaller artery that supplies the utricle, superior saccule, and ampulae of the anterior and lateral semicircular canals (Kim et al, 1999). The labyrinthine artery is an end-artery, and as such may be relatively more vulnerable than other circulations. Diagnosis may be difficult because the brain may show no lesion.
Main symptoms are ipsilateral cerebellar ataxias (middle and/or superior cerebellar peduncles), nausea and vomiting, slurred (pseudobulbar) speech, loss of pain and temperature over the opposite side of the body. Partial deafness, tremor of the upper extremity, an ipsilateral Horner syndrome and palatal myoclonus have been reported. Clinically, this stroke may be impossible to distinguish from a partial AICA or PICA territory stroke. It is much rarer than either one. Ocular pulsion away from the side of lesion has been reported in SCA syndrome. Diagnosis is via MRI.
This is a catastrophic event, typically a hypertensive bleed. It presents with of coma, quadriplegia, small reactive pupils and absent horizontal eye movements. In most quadriplegic patients a hematoma in the middle of the pons is centered at the junction of the tegmentum and basis pontis. Ocular bobbing is a less constant feature. Lateral tegmental hemorrhages present with 1 1/2 syndrome, small reactive pupils, limb ataxia of the cerebellar type, and contralateral hemisensory loss (Caplan and Goodwin, 1982). Diagnosis may be made via MRI or CT scan.
0.5% of all brain infarcts. Contralateral hemiparesis sparing the face, hemisensory loss of the posterior column type (contralateral). Weakness of the tongue ipsilateral to the infarct. Pathology may be in vertebral artery or mesial limb of vertebral artery after PICA. Upbeat nystagmus may occur. Small vessel disease (diabetes, hypertension, hypercholesterolemia) is the usual cause.
It is fairly common to encounter areas of increased signal on T2 MRI in the pons. These patients often display symptoms of disequilibrium, difficult with speech and swallowing. (Kwa et al, 1998). In the author's experience, these patients often exhibit rebound nystagmus, which is a variant of gaze-evoked nystagmus. Individuals with midline pontine infarcts usually have normal ABR testing (Faught and Oh, 1985)
Decreased blood flow in the vertebrobasilar system is invoked as a potential explanation for a myriad of symptoms possibly attributable to the brainstem. At this writing (2/1999), there is no well accepted way to establish this diagnosis. While MRI technology has advanced greatly, MRA is presently not of high enough resolution to reliably visualize the tiny arteries involved in this area. Conventional angiography is the most reliable way to infer the diagnosis.
As the basilar artery supplies most of the brainstem, occlusion is commonly catastrophic resulting in quadriplegia. Death from respiratory failure is common. The "locked in syndrome", denoting a state where the unfortunate patient can think and see but may be unable to respond may occur. Occlusion of the "top" of the basilar artery can result in a large number of complex syndromes that may include visual hallucinations, somnolescence, various ocular findings mainly involving vertical gaze and/or convergence/retraction nystagmus. The classic paper is by Kubik and Adams (1946) . Diagnosis is via MRI/MRA.
Usually manifests as PICA territory infarct (see below). Bilateral occlusions are much rarer than unilateral, and have a slowly progressive course and poor prognosis (Caplan, 1983). Diagnosis is via angiography combined with MRI.
Carotid disease rarely causes vertigo. This is because the parts of the brain that control motion perception are in the back, and are supplied by different arteries (the vertebral and basilar arteries). When carotid disease is severe, and accompanied by disease in the back arteries, carotid disease can be associated with vertigo, but this is unusual. Diagnosis is via MRA, doppler, or angiography.
The brainstem graphic is courtesy of Northwestern University.
|Eponym||Site||Cranial Nerves||Tracts||Signs||Usual Cause|
|Weber||Base of Midbrain||III||Corticospinal||Oculomotor palsy with crossed hemiplegia||Vascular, tumor|
|Claude||Midbrain tegmentum||III||Red nucleus and Brachium Conjunctivum||Oculomotor palsy with contralateral cerebellar ataxia and tremor||Vascular, tumor|
|Benedict||Midbrain tegmentum||III||Red nucleus, corticospinal tract, brachium conjunctivum||Oculomotor palsy, contralateral cerebellar ataxia, corticospinal signs||Vascular, tuberculoma, tumor|
|Nothnagel||Midbrain tectum||Unilateral or bilateral III||Superior cerebellar peduncles||Ocular palsies, paralysis of gaze, cerebellar ataxia||Tumor|
|Parinaud||Dorsal Midbrain||Paralysis of upward gaze and accommodation, fixed pupils, retraction nystagmus||Pinealoma, hydrocephalus|
|Millard-Gubler and Raymond-Foville||Base of Pons||VII and sometimes VI||Corticospinal tract||Facial and 6th palsy, contralateral hemiplegia, sometimes gaze palsy||Vascular,tumor|
|Avellis||Medulla tegmentum||X||Spinothalamic, sometimes pupillary fibers||Paralysis of soft palate and vocal cord and contralateral hemianesthesia||Infarct or Tumor|
|Jackson||Medulla Tegmentum||X,XII||Corticospinal||Avellis plus ipsilateral tongue||Infarct or Tumor|
|Wallenberg||Medulla, lateral tegmentum||Spinal V,IV,X,XI||Lateral STT,Descending Pupil fibers, Spinocerebellar and olivocerebellar tracts||Ipsi V, IV, X, XI palsy, Horner's, cerebellar ataxia. Contra pain and temp||Vascular - Pica or vertebral|