The main cause of motor weakness is damage to the primary crossed corticospinal tract. Most patients with stroke (80%-90%) have motor symptoms or signs. Hemiparesis with uniform weakness of the arm and leg associated with hemisensory deficit and speech deficit (dysphasia or dysarthria) usually indicates a large supratentorial lesion that involves the middle cerebral artery (MCA). Such patients have more severe weakness than do those with isolated hemiparesis. Crossed brainstem syndromes, well known with eponyms, are characterized by palsy of one of the 12 cranial nerve pairs associated with a contralateral neurological deficit due to involvement of the neurological long tracts (mainly motor or sensory). The integrity of all motor tracts, with the pyramidal tract as the main descending fiber bundle, but also the corticorubrospinal and corticoreticulospinal systems, appears to account for stroke recovery in a recent in vivo diffusion tensor imaging (DTI) study in chronic stroke patients.

The primary function of the sensory cortex is to discriminate sensation: appreciation and recognition of spatial relations, appreciation of similarity and differences of external objects, precise localization of the point touched, and identification of objects (stereognosis). Although less carefully examined than motor or speech abnormalities, somatosensory abnormality is present in at least half of stroke patients. The sensory abnormality is characterized by the presence of paresthesias and a selective loss of lemniscal sensation. Pontine tegmental strokes affecting the sensory tracts are often accompanied by sensory symptoms. Concomitant involvement of the adjacent pyramidal tract results in a sensory-motor stroke, and additional involvement of the cerebellothalamic fibers at the ventrolateral nucleus may produce a hypesthetic ataxic hemiparesis syndrome. Although motor symptoms are usually dominant in patients with subcortical strokes, small or even relatively large lesions primarily affecting the thalamocortical sensory radiation can result in pure or predominant sensory symptoms.

Ataxia is the most important sign of cerebellar disease, but there are other potential causes of ataxia. Postural and limb tremor are additional signs of cerebellar disease. Patients with cerebellar disorders may walk with a wide-based, staggering gait, making it seem as if they were intoxicated by alcohol. Frontal lobe disorders might cause cerebellar-like symptoms with walking difficulties and clumsiness. Frontal lobe lesions are commonly associated with impairment of cognitive function and changes in personality, and often cause urinary incontinence. Lesions of the cerebellar hemisphere are followed by ipsilateral limb ataxia including hypotonia in acute lesions, and if the dentate nucleus is involved, kinetic tremor. Vascular lesions of the cerebellum itself and of the corticopontocerebellar and dentatothalamic pathways might result in ataxia. Limb ataxia and ataxia of gait are common in superior cerebellar artery (SCA), the posterior inferior cerebellar artery (PICA), and the anterior inferior cerebellar artery (AICA) territory infarctions.

This chapter presents a brief background on the rationale for how the cerebellum is engaged in non-motor functions. It discusses the relationship of the cerebellar motor syndrome to the higher order aspects of cerebellar dysfunction. The chapter analyzes the nature of the neuro-behavioral deficits and their relationship to cerebellar structure and vascular anatomy. It examines the clinical relevance of the cognitive and behavioral manifestations of cerebellar stroke in the diagnosis and management of patients with posterior circulation ischemia. In stroke neurology, the natural and appropriate tendency is to consider stroke syndromes as manifestations of occlusions of specific blood vessels. Bedside and office-based tests that the neurologist can administer to detect the cerebellar cognitive affective syndrome (CCAS) should focus on the domains known to be affected, namely, disorders of executive function, visuospatial cognition, language-based tests, and assessment of affect and other neuropsychiatric domains.

The analysis of many different studies on the characteristics of headaches provides data to help predict the type of cerebrovascular disease according to headache patterns. Lack of headache at onset, sentinel headache, or associated vomiting is predictive of ischemic stroke. A history of throbbing headache is predictive of developing headache during a stroke. A headache preceding the cerebrovascular event (sentinel headache) has been a common occurrence in most studies, reported in up to 60% of patients. The coexistence of headache and stroke encompasses a large spectrum of possibilities, including stroke caused by migraine headache, migraine developing after a stroke, and non-migraine headache occurring in relation to stroke. A higher incidence of patent foramen ovale (PFO) in migraine with aura patients suggests that cardiac microemboli affecting the vertebrobasilar circulation may participate in the migrainous mechanisms of these patients.

This chapter discusses the main types of eye movement paralysis resulting from brainstem lesions, and the related pathophysiology. The abnormalities are easily detected at the bedside by studying three main types of eye movements: saccades; smooth pursuit; and the vestibular ocular reflex (VOR). The chapter reviews eye movement disturbances due to cerebellar and cerebral hemispheric lesions, resulting in relatively more subtle syndromes. The stroke-related lesions that most often involve horizontal gaze are located in the cerebral hemispheres and the pons. The hemispheral lesions are most often relatively large hemorrhages or infarcts that include the lateral aspect of the frontal lobe and/or the deep basal ganglia-capsular regions. Outside the brainstem, a number of suprareticular structures, located in the cerebellum and the cerebral hemispheres, control eye movements. Damage to these structures results in saccade and/or smooth pursuit disturbances usually much more subtle than those due to brainstem lesions.

This chapter discusses cortical visual defects in terms of primary deficits in visual field loss from damage to the geniculostriate pathway, and secondary deficits from damage to components of the ventral and dorsal streams. Incomplete bilateral hemianopia can be distinguished from bilateral ocular disease by the congruity of the visual loss and usually a step defect along the vertical meridian, the best clue to the hemifield nature of the loss. Bilateral lesions in the posterior portions of the cerebral hemispheres, including the occipital lobes, the posterior temporal lobes, and the inferior posterior parietal lobes, are surprisingly common. Astereopsis occurs in patients with bilateral occipitoparietal lesions. Less severe deficits occur with unilateral lesions. Other visuospatial dysfunction may be associated. Stereotests, which are cards viewed with different polarized or colored glasses worn by the two eyes, are required to measure deficient stereopsis.

Transient monocular visual loss is the most important visual symptom of arteriosclerotic vascular disease, arteritis and states of altered coagulability, and thrombocytosis. In most patients, the visual abnormality during each individual attack of visual loss is stereotypic. Visual loss occurrence is divided into four types. Type I is due to transient retinal ischemia, type II to retinal vascular insufficiency, and type III to vasospasm. Type IV occurs in association with antiphospholipid antibodies but includes cases of unknown etiology. Sudden monocular blindness is the major symptom of an ocular stroke causing permanent visual loss. The ocular strokes discussed are: central retinal artery (CRA) occlusion, ophthalmic artery (OA) occlusion, branch retinal artery (BRA) occlusion, and ischemic optic neuropathy (ION), which is the result of infarction of the optic nerve. Blindness can result from infarction of the retina or the optic nerve.

Physiological and clinical vestibular vertigo syndromes are commonly characterized by a combination of phenomena involving perceptual, oculomotor, postural, and vegetative manifestations: vertigo, nystagmus, ataxia, and nausea. Most of the central vestibular syndromes and some of the peripheral vestibular syndromes may have a vascular etiology. Episodic vertigo and oculomotor abnormalities are common early symptoms of reduced vertebrobasilar blood flow due to the steep pressure gradient from the aorta to the terminal pontine arteries. To date, at least eight subgroups of anterior inferior cerebellar artery (AICA) infarction have been identified according to the pattern of neurootological presentations, among which the most common is the combined loss of auditory and vestibular functions. Unilateral ischemic lesions of the pontomesencephalic vestibular pathways, which run along the medial longitudinal fasciculus (MLF), predominantly cause vestibular tone imbalance in the roll plane. Unilateral thalamic infarctions may cause contralateral falling, astasia, or contralateral ocular tilt reaction (OTR).

Many different conditions cause hearing impairment including inflammation, trauma, aging (presbyacusis), ototoxic drugs, genetic disorders, and stroke. As the blood supply to the auditory system originates from the vertebrobasilar system, hearing loss and tinnitus are common with vertebrobasilar territory ischemic stroke. This chapter reviews the clinical spectrum of hearing impairment associated with stroke. Central hearing impairment results from lesions central to the cochlear nucleus from the brainstem auditory nuclei to the auditory cortex in the temporal lobe. Central hearing abnormalities characterized by difficulty understanding spoken communication usually result from lesions of the central auditory pathways rostral to the cochlear nucleus. Brainstem stroke can cause auditory symptoms such as hearing loss, phantom auditory perceptions (tinnitus and hallucinations), and hyperacusis. Cortical deafness, pure word deafness, auditory agnosia for environmental sounds, and amusia are well-known central auditory disorders associated with hemispheric stroke.

Acute, paroxysmal, recurrent, transient, permanent, and delayed movement disorders are occasionally reported in patients during the acute phase of stroke, or as delayed syndromes months or years after an acute vascular lesion. This chapter provides an overview on hyperkinetic manifestations of stroke. Transient or paroxysmal hemichorea-hemiballism can be difficult to distinguish from limb shaking, and has occasionally been considered as a vertebrobasilar transient ischemic attack (TIA). Orofacial dyskinesias have been found in a few patients with brainstem infarcts, associated with palatal myoclonus in one patient, and after thalamic infarcts. Mental dystonia has been reported in association with a posteroventrolateral thalamic infarct. Head or cervical tremor can develop in bilateral thalamic and midbrain infarcts and in bilateral cerebellar infarcts. Unilateral asterixis has been reported with contralateral lesions involving any structure involved with motion, and also with lesions in the territory of the PCA and particularly in patients with ipsilateral brainstem stroke.

Stroke has long been recognized as one of the most common causes of epileptic seizures, particularly in older people. This chapter provides an overview of the various epidemiological studies on poststroke seizures (PSS) and poststroke epilepsy (PSE), and attempts to give an understanding of their pathogenesis, outcome, and management. The most consistent risk factors for PSS at stroke onset are size and cortical involvement. Abnormal electroencephalography's (EEGs) have been noted in up to 38% of patients with lacunar infarction, and lateralizing EEG abnormalities in over 80% of patients with early seizures in lacunar strokes also supports the concept of associated cortical infarction. Large, anterior circulation, ischemic strokes carry the highest risk of seizures. Patients who develop PSE usually require pharmacological treatment. Seizures following stroke occur in less than 10% of patients in the first few weeks after stroke.

Sleep-wake disturbances (SWD) are frequently (20%-50%) encountered in stroke patients. Clinical symptoms include hypersomnia, excessive daytime sleepiness, fatigue, and insomnia. The most dramatic forms of poststroke hypersomnia are observed in patients with bithalamic paramedian stroke. The presence of SWD after stroke is associated with cognitive and psychiatric (depression, anxiety) disturbances. The recognition and diagnosis of poststroke SWD occur primarily on clinical grounds. Validated questionnaires such as the Epworth Sleepiness Scale and the Fatigue Severity Scale may help in the recognition of poststroke sleepiness and fatigue. In patients with paramedian thalamic stroke, treatment with 20-40 mg of bromocriptine may improve apathy and presleep behavior. Changes in sleep architecture depend upon: patient and health characteristics present before the stroke, topography and extent of the lesion, associated complications of stroke (e.g. SDB, fever, infections, cardiovascular disturbances, depression, anxiety), drug treatment, and time after stroke onset.

Brainstem stroke due to an embolus to the basilar artery, is one of the most common causes of initially unexplained coma. This chapter explains why and how patients become comatose after an ischemic or hemorrhagic stroke. Acute coma from a stroke may be due to an embolus to the basilar artery destroying the ascending reticular formation in the dorsal pons and mesencephalon. The approach to a patient with coma and abnormal consciousness requires three steps. First, determine whether the patient is truly comatose and exclude confounders or misleading signs. Second, with a focused neurological examination, it is possible to localize the lesion using information on brainstem reflexes and motor responses to noxious stimuli. Third, breathing patterns, blood pressure, pulse, and temperature characteristics may also indicate a certain cause. Coma is expected in catastrophic and often fatal ganglionic cerebral or pontine hemorrhages.

Functional neuroimaging has contributed new insights in the field of aphasia research. Techniques like repetitive transcortical magnetic stimulation (rTMS), Wada testing, and cortical stimulation during neurosurgery with grid mapping, all of which inhibit distinct areas of the brain, have determined which nodes of the networks visualized in functional neuroimaging are critical for each function. The neurological examination of a patient with aphasia can be broken down into six major categories: naming, fluency, repetition, comprehension, reading, and writing. The classical aphasia syndromes result from the infarction of defined vascular distributions, each typically associated with a specific set of neurological deficits, also caused by damage to that particular region of the brain. Patients who develop aphasia following acute stroke typically recover well with only mild long-term language deficits. Many of the techniques currently employed by speech-language pathologists focus on treatment of the damaged component of the system.

The fundamental feature of delirium is disordered attention. Delirium is associated with a variety of medical illnesses including pneumonia, urinary tract infection, sepsis, meningitis, dehydration, congestive heart failure, uremia, liver failure, head injury, and postictal states. Increased mortality and morbidity are likely due to the seriousness of the underlying disease and the difficulty in caring adequately for very agitated patients who often cannot cooperate with treatments. Delirium can occur after an acute stroke and may even be the only observable neurological abnormality. The brain lesions in patients with abulia, when localizable, were located in the upper mesencephalic tegmentum, substantia nigra, medial thalami, striatum, and frontal lobes. Many of the lesions involved or interrupted projecting fibers to the frontal lobes. In contrast, when hyperactive agitated patients had focal brain lesions, the location was most often in the posterior portions of the cerebral hemispheres in the temporal, occipital, and inferior parietal lobes.

This chapter addresses both organizational and clinical aspects of the frontal lobes, particularly the signs, symptoms, and cerebrovascular lesion patterns. The frontal lobes comprise multiple functional entities and can be subdivided into three major divisions: primary motor, premotor, and prefrontal cortical areas. The cognitive, emotional, and behavioral domains of frontal lobe syndromes can be particularly challenging. Strokes involving the lateral primary motor and premotor cortices typically involve rostral branches (precentral and central artery) of the superior division of the middle cerebral artery (MCA). Although few studies have systematically analyzed the short and long-term outcome of patients with frontal lobe strokes, it is clear that there is a substantial role for health providers in managing and supporting the recovery. Variables influencing recovery include the location and extent of the cerebral damage, associated cognitive, motor, and emotional impairments, treatment services, and supportive care.