Caplan Syndrome: Caplan LR

Caplan LR. · Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. · Neurology. · Pubmed #16401854 No free full text.

Abstract: Many patients with congestive heart failure develop neurologic dysfunction. This may take the form of a cardiac encephalopathy that shares clinical features with other metabolic encephalopathies. The causes are multiple. There is a particular, previously unreported, syndrome that occasionally develops in some patients with congestive heart failure that resembles the findings in patients with normal pressure hydrocephalus. This syndrome is characterized by apathy and abulia with preserved alertness; it is caused by fluid retention within the cranial cavity. The syndrome may also develop in patients with other conditions that cause anasarca, e.g., severe liver or kidney disease or hypoalbuminemia. Because patients with these conditions are often quite ill, it has been difficult to verify the pathophysiologic aspects of the syndrome so that its mechanism must remain a hypothesis that awaits more definitive study in a series of patients. I have not seen this syndrome discussed in any cardiology or neurology texts or reports, and it seems to be completely unknown to cardiologists and neurologists. I have recognized about one patient per year with this syndrome.

Brandt T, Steinke W, Thie A, Pessin MS, Caplan LR. · Department of Neurology, University Hospital of Heidelberg, Germany. · Cerebrovasc Dis. · Pubmed #10773642 No free full text.

Abstract: Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.

Saposnik G, Noel de Tilly L, Caplan LR. · Stroke Research Unit, Division of Neurology, Department of Medicine, St Michael's Hospital, University of Toronto, 55 Queen St E, Ste 931, Toronto ONM5C1R6, Canada. · Arch Neurol. · Pubmed #18852355 No free full text.

Abstract: BACKGROUND: Little is known about stroke mechanisms in patients with fluctuating symptoms and the role of branch atherosclerotic disease. OBJECTIVE: To report a novel stroke presentation associated with a paramedian pontine infarct due to branch disease with a fluctuating course. DESIGN: Case report. SETTING: Academic research. Patient A 63-year-old man with hypertension, diabetes mellitus, and dyslipidemia was seen with fluctuating right-sided weakness and dysarthria. He had had 2 episodes of complete bilateral horizontal conjugate gaze palsy with unimpaired consciousness lasting for 5 minutes each. His pupils were 4 mm and were equal and reactive to light. Vertical gaze and convergence were preserved. His neurologic status fluctuated between 3 and 15 on the National Institutes of Health Stroke Scale. MAIN OUTCOME MEASURES: Results of computed tomographic angiography, perfusion, and magnetic resonance imaging. RESULTS: Intravenous tissue plasminogen activator was administered within a 3-hour window. Fluctuations in motor weakness persisted for 12 hours after receiving thrombolytic therapy. Neuroimaging showed an acute left paramedian pontine infarct with a patent basilar artery. CONCLUSIONS: Branch disease is a common mechanism in pontine infarctions. We coined the term "pontine warning syndrome" to characterize recurrent stereotyped episodes of motor or sensory dysfunction, dysarthria, or ophthalmoplegia associated with a high risk of imminent basilar artery branch infarction and a permanent deficit resembling those of capsular warning syndrome.