Stroke School for Internists – Part 1
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Cognitive Emotional Sequelae Post Stroke
11/26/2019 The Neuropsychology of Objectives 1. Identify various cognitive sequelae that may result from stroke Stroke: Cognitive & 2. Explain how stroke may impact emotional functioning, both acutely and long-term Emotional Sequelae COX HEALTH STROKE CONFERENCE BRITTANY ALLEN, PHD, ABPP, MBA 12/13/2019 Epidemiology of Stroke Stroke Statistics • > 795,000 people in the United States have a stroke • 5th leading cause of death for Americans • ~610,000 are first or new strokes • Risk of having a first stroke is nearly twice as high for blacks as whites • ~1/4 occur in people with a history of prior stroke • Blacks have the highest rate of death due to stroke • ~140,000 Americans die every year due to stroke • Death rates have declined for all races/ethnicities for decades except that Hispanics have seen • Approximately 87% of all strokes are ischemic an increase in death rates since 2013 • Costs the United States an estimated $34 billion annually • Risk for stroke increases with age, but 34% of people hospitalized for stroke were < 65 years of • Health care services age • Medicines to treat stroke • Women have a lower stroke risk until late in life when the association reverses • Missed days of work • Approximately 15% of strokes are heralded by a TIA • Leading cause of long-term disability • Reduces mobility in > 50% of stroke survivors > 65 years of age Source: Centers for Disease Control Stroke Death Rates Neuropsychological Assessment • Task Engagement • Memory • Language • Visuospatial Functioning • Attention/Concentration • Executive -
Lack of Motivation: Akinetic Mutism After Subarachnoid Haemorrhage
Netherlands Journal of Critical Care Submitted October 2015; Accepted March 2016 CASE REPORT Lack of motivation: Akinetic mutism after subarachnoid haemorrhage M.W. Herklots1, A. Oldenbeuving2, G.N. Beute3, G. Roks1, G.G. Schoonman1 Departments of 1Neurology, 2Intensive Care Medicine and 3Neurosurgery, St. Elisabeth Hospital, Tilburg, the Netherlands Correspondence M.W. Herklots - [email protected] Keywords - akinetic mutism, abulia, subarachnoid haemorrhage, cingulate cortex Abstract Akinetic mutism is a rare neurological condition characterised by One of the major threats after an aneurysmal SAH is delayed the lack of verbal and motor output in the presence of preserved cerebral ischaemia, caused by cerebral vasospasm. Cerebral alertness. It has been described in a number of neurological infarction on CT scans is seen in about 25 to 35% of patients conditions including trauma, malignancy and cerebral ischaemia. surviving the initial haemorrhage, mostly between days 4 and We present three patients with ruptured aneurysms of the 10 after the SAH. In 77% of the patients the area of cerebral anterior circulation and akinetic mutism. After treatment of the infarction corresponded with the aneurysm location. Delayed aneurysm, the patients lay immobile, mute and were unresponsive cerebral ischaemia is associated with worse functional outcome to commands or questions. However, these patients were awake and higher mortality rate.[6] and their eyes followed the movements of persons around their bed. MRI showed bilateral ischaemia of the medial frontal Cases lobes. Our case series highlights the risk of akinetic mutism in Case 1: Anterior communicating artery aneurysm patients with ruptured aneurysms of the anterior circulation. It A 28-year-old woman with an unremarkable medical history is important to recognise akinetic mutism in a patient and not to presented with a Hunt and Hess grade 3 and Fisher grade mistake it for a minimal consciousness state. -
Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
A.qxd 9/29/05 04:02 PM Page 1 A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis (i.e., with dorsal column disease). Cross References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circum- stances: normal old age obesity after abdominal surgery after multiple pregnancies in acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neu- rone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis. -
Lacunar Stroke
Lacunar Stroke Prior to making any medical decisions, please view our disclaimer. Clinical Lacunar Syndrome Lacunar strokes tend to occur in patients with diabetes, hyperlipidemia, smoking or chronic hypertension and may be clinically silent or present as pure motor hemiparesis, pure sensory loss, or a variety of well-defined syndromes (e.g., dysarthria-clumsy hand, ataxic- hemiparesis). Descending compact white matter tracts or brainstem gray matter nuclei are injured, often producing widespread and striking initial deficits. However, the prognosis for recovery with lacunar stroke is better than with large artery territory stroke, and for this reason many centers favor using antiplatelet therapy (aspirin, clopidogrel) or conservative management rather than thrombolytic therapy for uncomplicated lacunar stroke. The risk of hemorrhagic transformation or edema in these patients is extremely low. Because initial clinical presentation may be deceiving particularly in the posterior circulation, all patients presenting with acute ischemic symptoms should undergo some form of neurovascular imaging to establish large vessel patency (CTA, MRA, ultrasound or angiography). Management Algorithm Phase 1 Additional Diagnostic Testing • Consider fasting lipids, lipoprotein (a), B12, folate, homocysteine • If suspicious of large vessel atheroma producing penetrator infarction, refer to algorithm for Large Vessel disease Prevention of Acute Recurrent Stroke • Consider antiplatelet therapy (e.g., aspirin, clopidogrel, ticlopidine, persantine, integrilin, -
26 Aphasia, Memory Loss, Hemispatial Neglect, Frontal Syndromes and Other Cerebral Disorders - - 8/4/17 12:21 PM )
1 Aphasia, Memory Loss, 26 Hemispatial Neglect, Frontal Syndromes and Other Cerebral Disorders M.-Marsel Mesulam CHAPTER The cerebral cortex of the human brain contains ~20 billion neurons spread over an area of 2.5 m2. The primary sensory and motor areas constitute 10% of the cerebral cortex. The rest is subsumed by modality- 26 selective, heteromodal, paralimbic, and limbic areas collectively known as the association cortex (Fig. 26-1). The association cortex mediates the Aphasia, Memory Hemispatial Neglect, Frontal Syndromes and Other Cerebral Disorders Loss, integrative processes that subserve cognition, emotion, and comport- ment. A systematic testing of these mental functions is necessary for the effective clinical assessment of the association cortex and its dis- eases. According to current thinking, there are no centers for “hearing words,” “perceiving space,” or “storing memories.” Cognitive and behavioral functions (domains) are coordinated by intersecting large-s- cale neural networks that contain interconnected cortical and subcortical components. Five anatomically defined large-scale networks are most relevant to clinical practice: (1) a perisylvian network for language, (2) a parietofrontal network for spatial orientation, (3) an occipitotemporal network for face and object recognition, (4) a limbic network for explicit episodic memory, and (5) a prefrontal network for the executive con- trol of cognition and comportment. Investigations based on functional imaging have also identified a default mode network, which becomes activated when the person is not engaged in a specific task requiring attention to external events. The clinical consequences of damage to this network are not yet fully defined. THE LEFT PERISYLVIAN NETWORK FOR LANGUAGE AND APHASIAS The production and comprehension of words and sentences is depen- FIGURE 26-1 Lateral (top) and medial (bottom) views of the cerebral dent on the integrity of a distributed network located along the peri- hemispheres. -
Balin Bhatia Gadolinium Deposition Basal Ganglia
T1 weighted basal ganglia hyperintensities due to gadolinium deposition – a cautionary note Bettina Balint, MD1,2 and Kailash P. Bhatia, MD, FRCP1 1 Sobell Department of Motor Neuroscience and Movement Disorders UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom 2 Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany Corresponding author: Prof Kailash P. Bhatia Sobell Department of Motor Neuroscience and Movement Disorders UCL Institute of Neurology Queen Square WC1G 3BG London U.K. Tel: +44 02034488723 Email: [email protected] Correspondence Word count: 585; Character count title: 91; number of references: 5; number of figures: 0; Supplemental Data: 0 Disclosures: Dr Balint reports no conflict of interest. Prof Bhatia reports no conflict of interest. Full disclosures for the past 12 months unrelated to the present manuscript: K.P.B. receives royalties from Oxford University Press and a stipend for MDCP editorship, holds grants from NIHR RfPB, MRC Welcome Strategic grant (WT089698), PD UK (Ref. no.: G-1009) and Horizon 2020 EC grant Propag- Aging. He has received honoraria/financial support to speak/attend meetings or serve on advisory boards from Ipsen, Merz, Allergan, Teva Lundbeck pharmaceutical companies. Gadolinium-based contrast agents (GBCAs) have been widely used in clinical MR imaging since the late 1980ies. Overall, they were considered safe, apart from the well-known risk of nephrogenic systemic fibrosis, which could be counteracted by limitation of their use in patients with renal insufficiency. Now however, there have been a number of publications describing the dose-dependent deposition of Gadolinium in the brain, manifesting as high signal intensities on non-enhanced T1-weighted images particularly in the dentate nucleus and globus pallidus, but also in the thalamus and the pons.1-3 Gadolinium is a rare-earth metal. -
Definition of Stroke/Brain Attack
Definition of Stroke/Brain Attack Stroke II: • A syndrome caused by disruption in the flow of Diagnosis, Evaluation, and Prevention blood to part of the brain due to either: – occlusion of a blood vessel • ischemic stroke Lenore N. Joseph, MD – rupture of a blood vessel Neurology Service Chief, McGuire VAMC • hemorrhagic stroke Assistant Professor of Neurology • The interruption in blood flow deprives the brain VCU Health System of nutrients and oxygen resulting in injury to cells Medical College of Virginia in the affected vascular territory of the brain 1 2 Stroke: The Problem Stroke: The Problem • Third leading cause of death in US • Among 6 month or longer survivors: – after heart disease and cancer – 48% have a hemiparesis • 740,000 new strokes each year – 22% cannot walk • 4.5 million stroke survivors – 24-53% report complete or partial • Leading cause of disability in adults in US dependence for activities • $45.5 billion per year in the USA – 12-18% are aphasic • 1 of 6 Americans will be affected – 32% are clinically depressed – only 10% fully recover 3 4 Symptoms of Brain Attack: Symptoms of Brain Attack: Teach your patients! Teach your patients! • Sudden weakness, paralysis, or numbness of: • Sudden unexplained dizziness –face – especially when associated with other – arm and the leg on one or both sides of the neurologic symptoms body – unsteadiness • Sudden loss of speech, or difficulty speaking or – sudden falls understanding speech • Sudden severe headache and/or loss of • Sudden dimness or loss of vision consciousness – -
To Study the Incidence of Lacunar Infarcts in Patients with Acute Ischemic Stroke and Its Correlation with Carotid Artery Stenosis 1Harmanpreet Singh, 2Gurinder Mohan
CTDT 10.5005/jp-journals-10055-0045 ORIGINAL RESEARCH ARTICLE To Study the Incidence of Lacunar Infarcts in Patients with Acute Ischemic Stroke and its Correlation with Carotid Artery Stenosis 1Harmanpreet Singh, 2Gurinder Mohan ABSTRACT Stroke and its Correlation with Carotid Artery Stenosis. Curr Trends Diagn Treat 2018;2(2):88-91. Introduction: Stroke remains the second leading cause of death worldwide, after ischemic heart disease. Lacunar Source of support: Nil infarcts are small deep infarcts ranging from 2 to 20 mm in Conflict of interest: None size resulting from occlusion of a penetrating artery which accounts for approximately 25% of all ischemic strokes. The present study was undertaken to study the incidence of lacunar infarcts in patients with acute ischemic stroke and its INTRODUCTION correlation with carotid stenosis. Stroke remains the second leading cause of death world- 1 Materials and methods: This study was performed at the wide, after ischemic heart disease. Early diagnosis Department of Medicine at a tertiary-care hospital in Amritsar, and treatment is necessary to prevent mortality and Punjab, in 50 patients presenting with acute ischemic stroke morbidity. 2 Stroke or cerebrovascular accident is a clini- with or without lacunar syndrome. All patients were diagnosed cal syndrome, and has been defined by the World Health using diffusion-weighted imaging (DWI) on magnetic resonance imaging (MRI) of the brain. Carotid artery stenosis was measured Organization (WHO) as “rapidly developing clinical with duplex ultrasound. signs of focal (at times global) disturbance of cerebral function, lasting more than 24 hours or leading to death Results: Patients with acute ischemic stroke had a mean age of 61.36 ± 11.36 years. -
Blood Pressure Management in Stroke Patients
eISSN 2508-1349 J Neurocrit Care 2020;13(2):69-79 https://doi.org/10.18700/jnc.200028 Blood pressure management in stroke patients REVIEW ARTICLE Seung Min Kim, MD, PhD1; Ho Geol Woo, MD, PhD2; Yeon Jeong Kim, MD, PhD3; Bum Joon Kim, MD, PhD3 Received: October 15, 2020 Revised: November 14, 2020 1Department of Neurology, VHS Medical Center, Seoul, Republic of Korea Accepted: November 26, 2020 2Department of Neurology, Kyung Hee University School of Medicine, Seoul, Republic of Korea 3Department of Neurology, Asan Medical Center, Seoul, Republic of Korea Corresponding Author: Bum Joon Kim, MD, PhD Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43- gil, Songpa-gu, Seoul 05505, Korea Tel: +82-2-3010-3981 Fax: +82-2-474-4691 E-mail: [email protected] Hypertension is a major, yet manageable, risk factor for stroke, and the benefits of well-controlled blood pressure are well established. However, the strategy for managing blood pressure can differ based on the pathomechanism (subtype), stage, and treatment of stroke patients. In the present review, we focused on the management of blood pressure during the acute stage of intracerebral hemorrhage, subarachnoid hemorrhage, and cerebral infarction. In patients with cerebral infarction, the target blood pressure was discussed both before and after thrombolysis or other endovascular treatment, which may be an important issue. When and how to start antihyper- tensive medications during the acute ischemic stroke period were also discussed. In regards to the secondary prevention of ischemic stroke, the target blood pressure may differ based on the mechanism of ischemic stroke. -
Clinical Consequences of Stroke
EBRSR [Evidence-Based Review of Stroke Rehabilitation] 2 Clinical Consequences of Stroke Robert Teasell MD, Norhayati Hussein MBBS Last updated: March 2018 Abstract Cerebrovascular disorders represent the third leading cause of mortality and the second major cause of long-term disability in North America (Delaney and Potter 1993). The impairments associated with a stroke exhibit a wide diversity of clinical signs and symptoms. Disability, which is multifactorial in its determination, varies according to the degree of neurological recovery, the site of the lesion, the patient's premorbid status and the environmental support systems. Clinical evidence is reviewed as it pertains to stroke lesion location (cerebral, right & left hemispheres; lacunar and brain stem), related disorders (emotional, visual spatial perceptual, communication, fatigue, etc.) and artery(s) affected. 2. Clinical Consequences of Stroke pg. 1 of 29 www.ebrsr.com Table of Contents Abstract .............................................................................................................................................1 Table of Contents ...............................................................................................................................2 Introduction ......................................................................................................................................3 2.1 Localization of the Stroke ...........................................................................................................3 2.2 Cerebral -
Medial Frontal Syndrome
Gnosia synthesis of sensory impulses resulting in perception, appreciation and recognition of stimuli. Agnosia is inability to recognize the meaning of a sensory stimuli even though it has been perceived Apraxia inability to perform a familiar, purposeful motor act on command that the patient is able perform spontaneously Precentral cortex - strip immediately anterior to the central or Sylvian fissure Prefrontal cortex - extending from the frontal poles to the precentral cortex and including the frontal operculum, dorsolateral, and superior mesial regions Orbitofrontal cortex including the orbitobasal or ventromedial and the inferior mesial regions and Superior mesial regions containing, primarily, the anterior cingulate gyrus The dorsolateral frontal cortex is concerned with planning, strategy formation, and executive function. The frontal operculum contains the centre for expression of language. The orbitofrontal cortex is concerned with response inhibition Patients with superior mesial lesions affecting the cingulate cortex typically develop akinetic mutism. Patients with inferior mesial (basal forebrain) lesions tend to manifest anterograde and retrograde amnesia and confabulation. Motor strip (area 4) Supplementary motor area (area 6) Frontal eye fields (area 8) Cortical center for micturition Motor speech area Prefrontal area Main projection site for dorsomedial nucleus of thalamus Project to basal ganglia and substantia nigra 3 parts- dorsolateral, medial, orbitofrontal Organization of self ordered tasks Executive -
PICA Vertebral Artery
Joint Annual Meeting SNG|SSN Basel, October 10th, 2012 Vascular territories and clinical Syndromes of the Posterior Circulation PD Dr Patrik Michel Neurology Service, CHUV Unité Cérébrovasculaire Posterior circulation strokes are suggested by the acute RQVHWRI« 1. Vestibular symptoms 2. Visual symptoms 3. Bilateral or crossed manifestations 4. Decreased level of consciousness at onset 5. Amnesic syndromes 1. Vestibulo-ocular manifestations of posterior circulation strokes Vertigo & nystagmus Vertical diplopia Ocular tilt reaction ¾ Skew deviation ¾ Visual tilt Is the vertigo due to stroke ? checklist Consider VWURNHRU7,$LI« Acute spontaneous onset vertigo/imbalance Patient cannot walk anymore, even with help Acute associated acute hearing loss (Æ AICA) New or unusual headache Patients with vascular risk factors, elderly, cardiac sources Other central symptoms (patient) or signs (witness) ¾ Hiccup, dysarthria, new Horner, mild long tract sign, etc. On examination: ¾ Normal head thrust (Halmagyi) and cold calorics despite persistent vertigo ¾ « Central » type nystagmus (see next slide) Is the nystagmus due to stroke ? checklist A nystagmus is in general central if it is « Multidirectional gaze-evoked Vertical Pendular, convergence-retraction Dissociated Not accompanied by vertigo/nausea Not improved by visual fixation Not useful to differentiate central from peripheral : Conjugate horizontal or rotatory nystagmus Positional or not (exception: short, stereotyped in BPPV) Transitory or persistent Nystagmus due to stroke