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  1. Home
  2. Books
  3. Stroke Syndromes, 3ed
  • Cited by 12
  • 3rd edition
  • Edited by Louis R. Caplan, Beth Israel Deaconess Medical Center, Boston, Jan van Gijn, University Medical Center, Utrecht
Publisher:
Cambridge University Press
Online publication date:
August 2012
Print publication year:
2012
Online ISBN:
9781139093286
DOI:
https://doi.org/10.1017/CBO9781139093286
Subjects:
Neurology and Clinical Neuroscience, Medicine
Information

Book description

The first two editions of Stroke Syndromes were widely welcomed as authoritative reference works in the assessment and diagnosis of stroke. This revised and updated third edition remains the definitive guide to patterns and syndromes in stroke. A comprehensive survey of all types of neurological, neurophysiological and other clinical dysfunction due to stroke. The book contains descriptions of clinical problems encountered in stroke patients and their differential diagnosis, enhancing pattern recognition and enabling clinicians to differentiate between possible locations on the basis of symptoms and signs. The companion volume Uncommon Causes of Stroke completes this highly authoritative reference work which clinicians in neurology will find essential to the understanding and diagnosis of stroke.

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Contents

Page 2 of 3

Contents
  • Chapter 25 - Cardiac and autonomic manifestations of stroke
    pp 294-305
  • View abstract

    Summary

    Memory systems are usually divided in five main categories: semantic, episodic, primary, procedural, and perceptual representation systems. Both semantic and episodic memories are forms of long-term memory with an unlimited capacity. The arterial blood supply of anatomical structures involved in memory comes from different sources. Memory impairment after stroke results from the cumulative effects of stroke and preclinical Alzheimer's disease or to unrecognized preexisting dementia. Mild memory complaints are frequent in stroke survivors. Confusion and memory loss can also result from infarction of the inferior genu of the internal capsule. This syndrome features fluctuating alertness, inattention, memory loss, apathy, abulia, psychomotor retardation, and severe memory loss. Concerning the influence of treatment modalities on memory defects, there are no differences between early and late aneurysmal surgery. Objective memory impairment is more frequent after surgical than after endovascular treatment of the ruptured aneurysm.
  • Chapter 26 - Dysarthria
    pp 306-312
  • View abstract

    Summary

    With the widespread use of computerized tomography (CT), it has become evident that aphasia and other cortical syndromes can result from lesions limited to subcortical structures. Both single-photon emission computed tomography (SPECT) and positron emission tomography (PET) have shown that subcortical strokes are accompanied by important abnormalities of cortical metabolism and perfusion. Strokes in the basal ganglia and deep white matter tracts can produce disorders of oral and written language, apraxia, neglect, amnesia, apathy, and several other psychiatric disturbances. Multiple subcortical lacunar stroke and vascular white matter changes are associated with cognitive impairment, cognitive decline, depression, and dementia. Posterior hematomas, including the pulvinar and dorsal nuclei, are those most commonly associated with aphasia, because this is the only region of the thalamus connected with cortical language areas. Most of these subcortical lesions were located in the right hemisphere, indicating that right subcortical structures are dominant for hemispatial attention and intention.
  • Chapter 27 - Dysphagia and aspiration
    pp 313-318
  • View abstract

    Summary

    Although the right hemisphere is often referred to as the nondominant or minor hemisphere, this chapter delineates its dominant and lateralized contributions to various cognitive and behavioral functions, including language, emotions, facial recognition, nonverbal memory, visuospatial processing, behavioral and delusional syndromes, that are often complementary to the dominant and lateralized functions of the left hemisphere. The presence of persistent hemispatial neglect is associated with poor functional outcome as measured by the ability to live independently. Amnesias with temporally short retrograde deficits have been conceptualized as pure or core amnesias because they are usually not contaminated by other cognitive-behavioral disturbances, such as confabulation or frontal executive dysfunction. Agnosias are considered relatively rare disorders because, traditionally, they were described in patients following discrete bilateral lesions. Most studies have found that motor impersistence is observed more commonly after right- compared to left-sided hemispheric lesions, with many patients having a left hemiparesis.
  • Chapter 28 - Respiratory dysfunction
    pp 319-328
  • View abstract

    Summary

    The prevalence of poststroke dementia (PSD) varies largely according to the composition of cohorts, setting, and delay after stroke. The cognitive syndrome of vascular dementia (VaD) is characterized by: memory deficit, dysexecutive syndrome, slowed information processing, and mood and personality changes. Cortical VaD relates to large vessel disease, cardiac emboli, and hypoperfusion. It prominently shows cortical and corticosubcortical arterial territorial and distal field infarcts. The occurrence of dementia depends on two factors: the total volume of brain loss because of infarcts and hemorrhages, and the location of these lesions. Many instances of dementia occurring in stroke patients are probably the consequence of the cumulative effect of the cerebrovascular lesions, Alzheimer pathology, and white matter changes. Patients with dementia after stroke are significantly less often treated with aspirin or warfarin than nondemented patients. Trials of secondary prevention of stroke usually exclude patients with obvious dementia.
  • Chapter 29 - Arterial territories of the human brain
    pp 329-343
  • View abstract

    Summary

    Prospective studies of mood changes after stroke in large samples of patients may permit the delineation of the acute emotional behavioral changes that are markers for the delayed development of emotional disturbances. Mood disorders can be quantified using specifically designed scales, such as the Center for Epidemiological Studies-Depression (CES-D) or the Hospital Anxiety and Depression Scale (HADS), and may be predictors of the later development of depression. The standardized diagnostic criteria of the DSM-IV for mood disorders are appropriate for stroke, as poststroke depression has a similar symptomatic profile to primary depression. Fear and anxiety are common following stroke. Anxiety is the second most prevalent mood disorder following stroke, being found in 3.5%-24% of patients. Careful monitoring of stroke and measurement of monoamine metabolites and neuroexcitatory amino acids, may give a better understanding of the biological mechanism underlining poststroke emotional disturbances.
  • Chapter 30 - Middle cerebral artery territory syndromes
    pp 344-363
  • View abstract

    Summary

    Various kinds of agnosia may affect each perceptual modality (e.g. visual, auditory, or tactile). This chapter provides an overview of their manifestations, clinical assessment, and cerebral localization. Transformation agnosia is a deficit involving a particular inability to extract a 3D representation of objects seen from unusual perspectives or unusual lighting, while recognition is preserved for prototypical 2D views. Pure alexia as well as difficulties in color and face recognition are often associated. Three main subtypes of apraxia disorders described are limb gestures, orofacial gestures, and wholebody gestures, each with different degrees of difficulties. Orofacial apraxia is accompanied by nonfluent aphasia and ideomotor limb apraxia. Callosal disconnection signs result from an interruption of these fibers by damage to the corpus callosum itself or adjacent white matter. These signs reflect the fact that each hemisphere receives only contralateral sensory inputs and controls only contralateral motor output, but also has specialized processing capacities.
  • Chapter 31 - Anterior cerebral artery
    pp 364-374
  • View abstract

    Summary

    Stroke is a common disorder of the central nervous system, often with secondary or associated neuromuscular manifestations. Stroke-related neuromuscular manifestations include peripheral neuropathy, myopathy, and dysautonomia. This chapter reviews primary as well as secondary neuromuscular manifestations of stroke. Secondary changes in muscles, connective tissues, and peripheral nerves in limbs rendered paretic or spastic by stroke have been demonstrated with electrophysiological, biomechanical, and histopathological methods. Vasculopathy in neurofibromatosis (NF) is rare but is well characterized in the form of intracranial occlusive arterial disease, cervical arteriovenous fistula, and intracranial aneurysm. Hemiplegic atrophy has long been observed in both human subjects and in experimental subhuman primates after upper motor neuron (UMN) lesions. Cardiac arrhythmias including malignant ventricular tachyarrhythmias and atrioventricular (AV) conduction blocks have been frequently described within the first 24 hours after stroke and can cause sudden death.
  • Chapter 32 - Anterior choroidal artery territory strokes
    pp 375-386
  • View abstract

    Summary

    The recognition of cardiac complications after stroke is of essence for the clinician, as the anticipation of such can guide clinical management and significantly alter patient outcomes after stroke. This chapter focuses mainly on the effects of the brain on the heart, discussing the neuroanatomical and pathophysiological correlates of these conditions, and their clinical and management implications. Pathophysiologically, the major underlying mechanism for myocardial damage in contraction band necrosis is felt to be sudden entry of calcium into the myocytes. Calcium deficiency with loss of intracellular calcium, anoxia followed by reoxygenation of the electron transport system, ischemia followed by reperfusion, or opening of the receptor-operated calcium channels by excessive amounts of locally released norepinephrine can lead to the final common pathway to cell death. Hypertension has been consistently shown in the acute phase of cerebrovascular diseases, even in patients who do not have a prior history of hypertension.
  • Chapter 33 - Thalamic infarcts and hemorrhages
    pp 387-396
  • View abstract

    Summary

    Dysarthria is characterized by dysfunction of the structures implicated in the control, initiation, and coordination of speech output: lips, tongue, jaw, palate, and larynx, which are innervated by the facial, glossopharyngeal, vagal, and hypoglossal nerves. Lesions that cause dysarthria occur in one of several locations along the neuraxis. This chapter presents the clinical features of dysarthria resulting from stroke and its associated neurological signs. Ischemic lesions of the upper motor neuron system may be unilateral or bilateral, cortical or subcortical. Ischemic lesions in the vertebrobasilar territory can result in both upper and lower motor neuron involvement. Ataxic dysarthria is the result of lesions occurring in the territory of the superior cerebellar and posterior inferior cerebellar arteries. Dysarthria can follow ischemic lesions of the extrapyramidal system occurring in the vascular territories of the deep penetrating branches of the anterior and middle cerebral arteries.
  • Chapter 34 - Caudate nucleus infarcts and hemorrhages
    pp 397-404
  • View abstract

    Summary

    In several stroke survivors, swallowing improves over time, although in a sizeable minority dysphagia is longer lasting. All dysphagic patients, including those with temporary swallowing impairments, are at a substantial risk of developing pneumonia. This chapter reviews pertinent aspects of swallowing physiology, and the neuroanatomy and patterns of swallowing impairments with different stroke locations. The facial motor nucleus and its associated nerve control the labial and facial muscles and participate in the oral and pharyngeal phases of swallowing. Dysphagia is often apparent early after stroke onset and improves with time. It rarely occurs in isolation and is typically accompanied by other telltale signs of bulbar dysfunction such as dysarthria, facial weakness or numbness, impaired cough, or impairment of alertness. Dysphagia and aspiration in the lateral medullary syndrome usually occur with involvement of the rostral and dorsolateral parts of the medulla oblongata.
  • Chapter 35 - Posterior cerebral artery
    pp 405-418
  • View abstract

    Summary

    The study of respiratory dysfunction following a cerebrovascular event may permit localization of the neuroanatomical lesion. In addition, some respiratory dysfunctions are related to the etiology and the prognosis of stroke. This chapter reviews current knowledge regarding these associations. Unilateral hemispheric ischemic strokes appear to affect respiratory function to a modest degree. In contrast to cerebral hemispheric involvement, brainstem strokes may induce a more typical respiratory pattern, allowing more precise correlation between structure and function. Patients with severe obstructive sleep apnea (OSA) syndrome may develop ischemic stroke more frequently, as OSA syndrome with an apnea-hypopnea index (AHI) >30 was associated with stroke in an elderly population. The adverse effects of central hyperventilation may be related to arterial vasoconstriction induced by hypocapnia, leading to decrease in cerebral blood flow but also inducing impairment in cerebral autoregulation and cerebral arterial compliance.
  • Chapter 36 - Space-occupying supratentorial and infratentorial ischemic stroke
    pp 419-425
  • View abstract

    Summary

    The advent of neuroimaging has allowed clinicians to improve clinico-anatomical correlations in stroke patients. Arterial trunks supplying the brainstem include: the vertebral artery, basilar artery, anterior and posterior spinal arteries, posterior inferior cerebellar artery, anterior inferior cerebellar artery, superior cerebellar artery, posterior cerebral artery, and anterior choroidal artery. The arterial supply of the medulla oblongata comes from the vertebral arteries that form the middle rami of the lateral medullary fossa, the posterior inferior cerebellar artery that gives rise to the inferior rami of the lateral medullary fossa, and the anterior and posterior spinal arteries. Different arterial trunks supply blood to the pons, including the vertebral arteries, anterior inferior cerebellar artery, superior cerebellar artery, and basilar artery. The leptomeningeal arteries consist of the terminal branches of the anterior, middle, and posterior cerebral arteries forming an anastomotic network on the surface of the hemispheres.
  • Chapter 38 - Midbrain infarcts and hematomas
    pp 439-447
  • View abstract

    Summary

    The middle cerebral artery (MCA) and its branches are the most commonly affected brain vessels in cerebral infarction. Prior to the introduction of imaging in living patients, semiology was a prominent factor in neurological research and practice. Many syndromes reflected inspired guesses, confirmed or denied by autopsy data, such postmortem observations often having been obtained long after the acute clinical event. The orbitofrontal branch supplies the orbital portion of the middle and inferior frontal gyri and the inferior orbital part of the frontal lobe. Middle cerebral artery inferior (or posterior) division territory infarcts represent 14% of 2000 patients of the Lausanne Stroke Registry. The posterior parietal and angular arteries may arise individually from the superior or the inferior division. The centrum ovale (or centrum semiovale) of Vieussens comprises the central white matter of the cerebral hemispheres, including the most superficial part of the corona radiata and the long association bundles.
  • Chapter 39 - Pontine infarcts and hemorrhages
    pp 448-460
  • View abstract

    Summary

    The anterior cerebral artery (ACA) arises as the medial branch of the bifurcation of the internal carotid artery (ICA) at the level of the anterior clinoid process. The ACA supplies the whole of the medial surfaces of the frontal and parietal lobes, the anterior four-fifths of the corpus callosum, the frontobasal cerebral cortex, the anterior diencephalon, and other deep structures. Ischemic stroke in the ACA territory is most often the result of emboli from the heart or the ICA. Transient loss of consciousness has been described in patients with ACA territory infarctions, but it is uncommon; sustained unresponsiveness most often indicates abulia or akinetic mutism. Anterograde amnesia has been known to follow rupture and related surgery for an anterior communicating artery (ACoA) aneurysm. Distinct syndromes of callosal disconnection resulting from ACA territory infarctions include ideomotor apraxia, agraphia, and tactile anomia restricted to the left hand in right-handed patients.
  • Chapter 40 - Medullary infarcts and hemorrhages
    pp 461-468
  • View abstract

    Summary

    Anterior choroidal artery (AChA) territory infarcts represent the second most common infarct in the territory of the deep perforators of the carotid artery system. The classical pattern of clinical signs attributed to AChA territory infarction is hemiplegia, hemianesthesia, and homonymous hemianopia, often associated with neuropsychological signs. Aphasia, spatial neglect, attention disorder, executive functioning impairment, and delayed memory are reported to be less severe than when due to thalamic or cortical infarctions. The high prevalence of arterial hypertension or diabetes mellitus as an isolated risk factor of stroke in small-sized AChA infarcts suggests that small artery disease is a common etiology of AChA territory infarcts. The clinical syndromes, vascular risk factor profile, presumed etiology of stroke, and prognosis allow consideration of small and large AChA territory infarcts in the differential diagnosis of patients with brain ischemia.
  • Chapter 41 - Cerebellar infarcts
    pp 469-479
  • View abstract

    Summary

    Anatomically, each thalamus lies rostral to the brainstem, lateral to the third ventricle, and medial to the internal capsule. As most blood to the thalamus arrives from the tip of the basilar artery and the proximal portions of the posterior cerebral arteries (PCAs), thalamic lesions may be associated with simultaneous lesions in the midbrain or in the distal territory of the PCA. Microangiopathy is the cause of most lateral thalamic infarcts although embolic sources are occasionally found. Large thalamic hemorrhages involve more nuclei and tracts, with or without ventricular extension, resulting in overlapping clinical syndromes. Common features seen in patients with thalamic hemorrhages include rapid onset of symptoms, inconstant impairment of consciousness even in large size hematomas, and a relatively good prognosis as compared with that for hemorrhages in the pons and basal ganglia. Venous thrombosis of the deep cerebral venous system usually leads to bilateral thalamic edema.
  • Chapter 42 - Borderzone infarcts
    pp 480-500
  • View abstract

    Summary

    The basal ganglia (BG) including the caudate nucleus are well known for their motor functions. The BG nuclei are anatomically and functionally associated with each of the frontal-striatal-thalamic-frontal circuits or loops. The caudate nucleus assumes the shape of a comet, curving along the lateral wall of the lateral ventricle. The caudate nucleus receives its blood supply mainly through the deep penetrators arising from the anterior cerebral arteries (ACAs) and middle cerebral arteries (MCAs) although there are individual differences. The major risk factors for caudate nucleus infarcts are: hypertension, hypercholesterolemia, diabetes mellitus, previous myocardial infarct, and cigarette smoking. As caudate nucleus infarcts can develop from any stroke mechanisms including lipohyalinosis, branch atheromatous disease, large artery atherothrombosis, or embolism, treatment of patients with caudate nucleus infarcts depends on the underlying stroke mechanism. Caudate nucleus hemorrhages account for approximately 7% of all intracerebral hemorrhages (ICH) and are caused by rupture of penetrating arteries.
  • Chapter 43 - The classical lacunar syndromes
    pp 501-508
  • View abstract

    Summary

    The posterior cerebral arteries (PCAs) are the major sources of blood supply to the midbrain, thalamus, occipital lobes, inferior and medial temporal lobes, and portions of the posterior inferior parietal lobes. The PCAs originate from the terminal bifurcation of the basilar artery, encircle the midbrain, and then divide into cortical branches as they reach the dorsal surface of the midbrain. Patients with PCA stenosis may have transient ischemic attacks (TIAs) alone, or they may precede infarction. The main clinical feature distinguishing proximal PCA occlusion from the other types of PCA strokes is hemiplegia. Unilateral and bilateral PCA territory infarctions can also result from mass lesions that cause transtentorial herniation and increased intracranial pressure. The temporal and calcarine artery branches are most often involved. Patients with bilateral infarctions involving the lingual and fusiform gyri in the inferior portions of the temporal lobes often manifest a restless, hyperactive state.
  • Chapter 44 - Basal ganglionic hemorrhages
    pp 509-515
  • View abstract

    Summary

    Severe ischemic stroke with progressive edema development is frequently life-threatening and associated with a poor prognosis due to limited expandability within the cranial cavity. This chapter describes the relevant aspects of supra- and infratentorial space-occupying strokes with particular emphasis on the role of decompressive surgery. Large ischemic infarction of the middle cerebral artery (MCA) territory can lead to a clinical syndrome called malignant MCA stroke. Cranial computed tomography (CT) is still the most widely used radiological modality to diagnose and monitor malignant MCA infarction. The only specific treatment option for this type of stroke with a solid base of evidence and major impact on the clinical course to date is decompressive surgery, that is, hemicraniectomy. Swelling of a large space-occupying cerebellar infarct appears within a few days from symptom onset and can lead to compression of the brainstem and midbrain or cause a hydrocephalus.
  • Chapter 45 - Lobar hemorrhages
    pp 516-525
  • View abstract

    Summary

    This chapter reviews the current literature on the frequency and causes of multiple brain infarcts, particular clinical and/or topographical patterns that suggest specific underlying mechanisms, and etiologies. The presence of multiple lacunar infarcts is an important prognostic indicator not only for functional recovery but also for a higher rate of recurrence. Various underlying conditions associated with multifocal involvement of the cerebral vasculature and/or a high rate of recurrent strokes may be responsible for multiple brain infarcts. Acute multiple infarcts may involve both hemispheres and may suggest some specific clinical pictures, particular causes, such as large artery disease, cardioembolism, angiitis, hematological disorders, hemodynamic mechanisms, or venous infarcts. In patients with simultaneous multiple, bihemispheric, and multilevel infarcts, most causes seem to be of similar type. Simultaneous multiple and multilevel infarcts may be associated with specific neurocognitive/psychological dysfunction patterns in most of the patients, allowing diagnosis accuracy.
  • Chapter 46 - Intraventricular hemorrhage
    pp 526-533
  • View abstract

    Summary

    The arterial system supplying the midbrain is terminal for the midbrain itself, arising from the basilar artery and from the bifurcation of the basilar artery. According to magnetic resonance imaging (MRI)-based stroke registries, the midbrain was involved in 0.9% of strokes and 3% to 8% of posterior circulation infarcts. Oculomotor palsies are frequent in midbrain strokes and dominate the neurological picture. Combined upward- and downward-gaze palsy has been related to bilateral or unilateral midbrain infarcts. A lacunar infarct of the lateral midbrain affecting the pyramidal tract in the cerebral peduncle can cause pure motor stroke. Midbrain hematomas or infarcts that involve the sensory lemniscus have been reported as causes of pure sensory strokes. Bilateral, isolated small infarcts in the lateral midbrain involving the corticospinal tracts have been responsible for tetraplegia and mutism, leaving conscious patients with only gaze movements as a means to communicate.
  • Chapter 47 - Subarachnoid hemorrhage syndromes
    pp 534-541
  • View abstract

    Summary

    Atheromatous stenosis of the basilar artery (BA) can cause pontine infarctions by superimposed thrombosis, which occlude the BA itself or the orifices of the branches of the BA. Pontine infarctions can occur following large thromboembolism lodging at the BA lumen. Emboli usually lodge in the distal portion of the BA, occluding the superior cerebellar artery (SCA) or orifices of branches of the distal BA. Lipohyalinosis and branch atheromatous disease of the penetrating small arteries are the major vascular pathologies in most patients who develop pontine infarction. Pontine infarctions are caused by a variety of vascular pathologies that can develop in large brain-supplying arteries. About 10% of all brain hemorrhages occur in the pons. Before the development of computed tomography (CT) scanning, primary pontine hemorrhages (PPH) were considered a uniformly fatal disease characterized by horizontal gaze paresis, pinpoint pupils, high fever, quadriparesis, and rapid onset of coma.
  • Chapter 48 - Cerebral venous thrombosis
    pp 542-553
  • View abstract

    Summary

    Since the first description of Wallenberg's syndrome more than 100 years ago, clinical and pathological findings of lateral medullary infarction (LMI) have been sporadically reported. Dizziness and ataxia are one of the most common symptoms/signs of lateral medullary infarction (LMI). Other symptoms/signs include nystagmus and ocular motor abnormality, dysphagia, dysarthria, hoarseness, nausea/vomiting, and hiccup. In patients with normal angiographic findings, atherothrombotic occlusion of a perforating artery itself seems to be the mechanism of infarction. Medial medullary infarction is usually caused by occlusion of penetrating branches associated with an atherosclerotic distal vertebral artery (VA) or vertebral arteries-basilar artery (VA-BA) junction. Lateral and medial medullary infarction may occur simultaneously or consecutively. Spontaneous primary medullary hemorrhage is rare. Although the causative role of hypertension is controversial, autopsy and imaging studies illustrate that hypertensive medullary hemorrhage does exist. Cavernous angiomas are a relatively frequent cause of medullary hemorrhage.
  • Chapter 49 - Carotid occlusion syndromes
    pp 554-559
  • View abstract

    Summary

    The most common locations for cerebellar infarcts are the posterior inferior cerebellar artery (PICA) and superior cerebellar artery (SCA) territories and they are about equally involved. Cerebellar infarcts are often characterized by associated non-specific symptoms, transposing into clinical conditions difficult to diagnose. The clinical presentation of ischemia in the territories of the various cerebellar arteries depends on whether the ischemia affects only the cerebellum, only the brainstem, or a combination of brainstem and cerebellum. The most common symptoms are vertigo or dizziness, vomiting, abnormal gait, headache, and dysarthria. The SCA infarcts often provoke edema with brainstem compression and herniation of the cerebellar tonsils. Cerebellovestibular signs are prominent in patients with partial occlusion of the SCA territory. Dysarthria is a characteristic symptom of SCA territory infarction. Pseudotumoral infarcts are responsible for the development of increased pressure within the posterior fossa and intracranially and may mimick posterior fossa tumors.
  • Chapter 50 - Cervical artery dissections
    pp 560-565
  • View abstract

    Summary

    Low-flow infarctions, also called borderzone infarctions, are considered the result of critically reduced cerebral perfusion pressure (CPP) in far-downstream brain arteries that causes critically compromised cerebral blood flow and insufficient oxygen supply in certain vulnerable brain areas. Transhemispheric and interterritorial collateral blood flow via the anterior and posterior communicating arteries and their individual distributions must be considered with respect to the site and size of borderzone infarctions. Cardiac arrest and hypotension can also cause low-flow infarcts that are usually bilateral. Although hypoxic-ischemic cerebellar damage is often found at necropsy, clinical signs of cerebellar dysfunction are rare and are usually overshadowed by cerebral abnormalities. The general medical prognosis of patients with low-flow infarcts is poor. Deaths as a result of cardiovascular complications are frequent and account for about 10% of deaths per year. An important diagnostic improvement in identifying low-flow infarcts was the use of rCBF techniques.
  • Chapter 51 - Intracranial arterial dissections
    pp 566-573
  • View abstract

    Summary

    A small number of syndromes that initially were correlated, more or less convincingly, with relevant lacunes observed at subsequent autopsy have come to be regarded as the classical lacunar syndromes (LACS), pure motor stroke (PMS), pure sensory stroke (PSS), homolateral ataxia and crural paresis (HACP), dysarthria-clumsy hand syndrome (DCHS), ataxic hemiparesis (AH), and sensorimotor stroke (SMS). The original cases of HACP were described as having weakness of the lower limb, particularly the ankle and toes, a Babinski sign, and striking dysmetria of the arm and leg on the same side. The classical LACS are clinical paradigms that should be fine-tuned by clinicians. They have been shown to be simple and reasonably valid markers for a numerically significant and pathophysiologically distinct subgroup of patients with cerebral infarction. Clinical and research utility of the classical LACS will have to be kept under review in the era of hyperacute stroke assessment and treatment.
  • Chapter 52 - Syndromes related to large artery thromboembolism in the posterior circulation
    pp 574-592
  • View abstract

    Summary

    This chapter describes the classification of basal ganglionic hemorrhages (BGHs) and the clinical features and prognosis of each type. The BGH is classified into six regional types according to the arterial territories of the presumed primary bleeding focus of the hematomas: anterior type; middle type; posteromedial type; posterolateral type; lateral type; and massive type. The characterization of each individual type is discussed in the chapter. The prognosis of BGH depends on age, hematoma volume, initial neurological status, presence of intraventricular blood, presence of hematoma expansion, and quality of care in patients with spontaneous intracranial hemorrhage (ICH). General principles of medical care of patients with an ICH apply to all patients with BGHs. They include intracranial pressure (ICP) control with ICP monitoring, blood pressure (BP) management, and blood sugar level control. For most of the patients with the middle, posteromedial, or lateral type of BGH, medical management is enough.
  • Chapter 53 - Spinal stroke syndromes
    pp 593-607
  • View abstract

    Summary

    Lobar intracerebral hemorrhages (ICHs) involve the white matter of the cerebral lobes, and originate at the corticosubcortical gray matter-white matter junctions. Lobar hemorrhages are distinct from other forms of ICH in their clinical presentation, causes, prognosis, and management. Lobar hemorrhage has been thought to have a better prognosis than the deep hemispheric (putaminal, thalamic) and posterior fossa hemorrhages. The case fatality rates reported have ranged between 11% and 32%, in comparison with 42% for basal ganglionic and thalamic ICH, and 43% for posterior fossa hemorrhages. The observed differences in case fatality between lobar and deep ICH probably reflect variations in hematoma size and mass effect more than their superficial versus deep location. The value of medical and surgical therapy for lobar ICH will ultimately have to be determined by clinical trials involving randomization of comparable groups of patients to one or the other type of treatment.

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