DOCSLIB.ORG

Handbook on Clinical Neurology and Neurosurgery

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Alekseenko YU.V. HANDBOOK ON CLINICAL NEUROLOGY AND NEUROSURGERY FOR STUDENTS OF MEDICAL FACULTY Vitebsk - 2005 УДК 616.8+616.8-089(042.3/;4) ~ А 47 Алексеенко Ю.В. А47 Пособие по неврологии и нейрохирургии для студентов факуль­ тета подготовки иностранных граждан: пособие / составитель Ю.В. Алексеенко. - Витебск: ВГМ У, 2005,- 495 с. ISBN 985-466-119-9 Учебное пособие по неврологии и нейрохирургии подготовлено в соответствии с типовой учебной программой по неврологии и нейрохирургии для студентов лечебного факультетов медицинских университетов, утвержденной Министерством здравоохра­ нения Республики Беларусь в 1998 году В учебном пособии представлены ключевые разделы общей и частной клиниче­ ской неврологии, а также нейрохирургии, которые имеют большое значение в работе врачей общей медицинской практики и системе неотложной медицинской помощи: за­ болевания периферической нервной системы, нарушения мозгового кровообращения, инфекционно-воспалительные поражения нервной системы, эпилепсия и судорожные синдромы, демиелинизирующие и дегенеративные поражения нервной системы, опу­ холи головного мозга и черепно-мозговые повреждения. Учебное пособие предназначено для студентов медицинского университета и врачей-стажеров, проходящих подготовку по неврологии и нейрохирургии. if' \ * /’ L ^ ' i L " / УДК 616.8+616.8-089(042.3/.4) ББК 56.1я7 б.:: удгритний I ISBN 985-466-119-9 2 CONTENTS Abbreviations 4 Motor System and Movement Disorders 5 Motor Deficit 12 Movement (Extrapyramidal) Disorders 25 Ataxia 36 Sensory System and Disorders of Sensation 46 Disorders of Cranial Nerves Functions 60 Cerebral Cortex and Neuropsychological Disorders 119 Dementia and Amnestic Syndromes 146 Coma 168 Intracranial Pressure, Cerebral Oedema, Hydrocepha­ 178 lus Headache and Facial Pain 198 Meningitis and Encephalitis 222 Peripheral Nerves Lesions 242 Stroke and Vascular Dementia 279 Epilepsy, Seizure and Syncope 328 Multiple Sclerosis and Demielinating Diseases 354 Amyotrophic Lateral Sclerosis 370 Spinal Cord Disorders 376 Movement Disorders 387 Myasthenia Gravis 412 Myopathic Disorders 417 Traumatic Brain Injury 421 Brain Tumours 447 Lumbar Disc Disease 463 Neurologic Examination 470 Lumbar Puncture 490 Literature 495 3 ABBREVIATIONS ADC Activated diffusion coefficients AIDS Immunodeficiency syndrome AVM Arteriovenous malformation BDNF Brain-derived neurotrophic factor CBF Cerebral blod flow CCF Carotid-cavernous fistulae CNS Central nervous system CSF Cerebrospinal fluid CT Computed tomography DWI Diffusion-weighted imaging EEG Electroencephalography EMG Electromyogram ESR Erythrocyte sedimentation rate GCS Glasgow coma scale HBO Hyperbaric oxygen HMSN Hereditary motor and sensory neuropathies ICH Intracerebral haemorrhage ICP Intracranial pressure MLF Medial longitudinal fasciculus MR1 Magnetic resonance imagine MRN Magnetic resonance neurography MS Multiple sclerosis NCS Nerve conduction studies NGF Nerve growth factor PCNSL Primary CNS lymphoma PNET Primitive neuroectodermal tumor SABP Systemic arterial blood pressure SAH Subarachnoid haemorrhage SIADH Syndrome of inappropriate secretion of antidiuretic hormone SLE Systemic lupus erythematosus SMA Supplementary motor area SSEP Somatosensory evoked potential STN Subthalamic nucleus TBI Traumatic brain injury 4 MOTOR SYSTEM AND MOTOR DISORDERS The spinal cord anterior horn cells are influenced by descending pathways from the cerebral cortex and from brainstem centres. These motor cortical and brainstem outflow areas are regulated by other cortical areas, the basal ganglia and cerebellum. The basal ganglia and the cerebellum are both characterized by parallel processing of inputs from cortical areas and subsequent projection back to cortex via thalamic relay nuclei. MOTOR CORTEX There are several motor cortical areas in the human; these are classified simply as the primary motor cortex, lateral pre-motor cortex, supplementary mo­ tor area (SMA), and motor regions of the cingulate cortex. The primary motor cortex (Brodmann's area 4) pyramidal cells are the principal source of the pyramidal tract but also project to other motor cortical areas and to sensory cortex, the thalamus, the basal ganglia (corpus striatum), the red nucleus, brainstem reticular nuclei, and the cerebellum (via the cortico­ pontine fibres and pontine nuclei). The primary motor cortex shows a soma- totopic organization but pyramidal cells may activate more than one muscle and a muscle may be affected by pyramidal cells spread over a wide cortical area. Primary motor cortex cells are activated prior to and during voluntary contralat­ eral movement, as shown by functional imaging and neurophysiological event- related recordings. Lesions of the primary motor cortex are associated princi­ pally with deficits of small accurate finger and hand movements. Such move­ ments require motor cortex outputs not only to agonist muscle spinal motor neu­ rons but also those needed to regulate the activity of antagonists and muscles needed to stabilize proximal joints. The lateral pre-motor cortex (the lateral part of Brodmann's area 6) is lo­ cated on the lateral aspect of the frontal lobe, anterior to the primary motor cor­ tex. There are two discreet motor areas (superior and inferior) within the lateral premotor cortex with separate motor cortical maps and corticospinal projections. There is a considerable output from the lateral pre-motor cortex to the medial brainstem tegmentum which projects to the spinal cord in the ventromedial de­ scending system (see below). The pre-motor cortex is important for the control of axial and proximal limb movements and also for the control of movements in response to external cues or instructions. The activation of the lateral pre-motor cortex begins prior to the execution of movement, suggesting an important role in preparation for movement, and may be bilateral. Lesions of the lateral pre­ 5 motor area produce proximal limb weakness and impairment of movements re­ quiring use of the whole arm and hand. There is also impaired learning of motor responses to external cues. The SMA (medial part of Brodmann's area 6) is on the inner aspect of the frontal lobe, anterior to area 4 and continuous with the lateral pre-motor cortex. The SMA receives considerable basal ganglia inputs and has outputs to the pri­ mary motor cortex, corticospinal tract, basal ganglia, cerebellum, red nucleus, and reticular formation. Like the lateral pre-motor cortex, the SMA seems to be important for the preparation of movements, particularly internally generated, learned, sequential, or bimanual movements. SMA lesions lead to difficulty ini­ tiating speech and movement, impaired bimanual co-ordination, and the 'alien limb' phenomenon where the arm moves spontaneously in response to external stimuli, grasping at objects spontaneously. This may represent a dissociation of externally (lateral pre-motor cortex) and internally (SMA) cued movement. Cingulate motor areas have been identified in humans and non-human primates. They have outputs to spinal cord and the basal ganglia and receive in­ puts from frontal pre-motor cortex. Cingulate motor neurons are active in inter­ nally generated movements and cingulate activation is seen mainly with com­ plex motor tasks. Stimulation of cingulate cortex produces complex motor activ­ ity. The descending pathways The descending pathways are grouped into two divisions within the spinal cord. A dorso-lateral group contains the lateral corticospinal tract along with the rubrospinal tract and the crossed reticulospinal tract (from the lateral pontine tegmentum). These dorso-lateral pathways are concerned with distal move­ ments. The ventro-lateral group is made up of the ventral corticospinal tract with the interstitiospinal, vestibulospinal, and reticulospinal (from medial pontine and medullary tegmentum) tracts and is involved in the control of proximal move­ ments. The pyramidal tract comprises the corticobulbar and corticospinal tracts and in the human, the latter component contains about one million fibres on each side. About 60 per cent of the fibres in the corticospinal tract originate in the frontal motor areas. The remainders are from parietal and somatosensory cortex. The corticospinal tract influences spinal afferent pathways, inhibitory interneu­ rons, and gamma efferent cells as well as the alpha motor neurons. There is con­ siderable convergence and divergence within the corticospinal tract; cortical py­ ramidal cells project to several muscles and each muscle can be activated by cells from a large cortical motor field. Direct synapses with alpha motor neurons are particularly dense on cells concerned with finger movements and there is a close association between the corticospinal tract and the execution of fine finger movements. Lesions of'the pyramidal tract tend to produce impaired manual dexterity with variable degrees of weakness. 6 Other descending pathways are poorly understood in man. The reticu­ lospinal pathway appears to be important in the startle reflex. Vestibulospinal pathways are concerned in part with postural control. THE CEREBELLUM AND BASAL GANGLIA Neither the cerebellum nor the basal ganglia have direct efferent connec­ tions to the spinal motor apparatus and yet both are clearly involved in the cor­ rect execution and control of movement. Profound disturbances of movement as their primary symptoms we can find in patients with lesions of these structures. Anatomically, both structures are characterized by extensive inputs from the cerebral cortex, parallel internal
Recommended publications
  • Brain Death and the Cervical Spinal Cord: a Confounding Factor for the Clinical Examination

    Brain Death and the Cervical Spinal Cord: a Confounding Factor for the Clinical Examination

    Spinal Cord (2010) 48, 2–9 & 2010 International Spinal Cord Society All rights reserved 1362-4393/10 $32.00 www.nature.com/sc REVIEW Brain death and the cervical spinal cord: a confounding factor for the clinical examination AR Joffe, N Anton and J Blackwood Department of Pediatrics, Stollery Children’s Hospital, University of Alberta, Edmonton, Alberta, Canada Study design: This study is a systematic review. Objectives: Brain death (BD) is a clinical diagnosis, made by documenting absent brainstem functions, including unresponsive coma and apnea. Cervical spinal cord dysfunction would confound clinical diagnosis of BD. Our objective was to determine whether cervical spinal cord dysfunction is common in BD. Methods: A case of BD showing cervical cord compression on magnetic resonance imaging prompted a literature review from 1965 to 2008 for any reports of cervical spinal cord injury associated with brain herniation or BD. Results: A total of 12 cases of brain herniation in meningitis occurred shortly after a lumbar puncture with acute respiratory arrest and quadriplegia. In total, nine cases of acute brain herniation from various non-meningitis causes resulted in acute quadriplegia. The cases suggest that direct compression of the cervical spinal cord, or the anterior spinal arteries during cerebellar tonsillar herniation cause ischemic injury to the cord. No case series of brain herniation specifically mentioned spinal cord injury, but many survivors had severe disability including spastic limbs. Only two pathological series of BD examined the spinal cord; 56–100% of cases had upper cervical spinal cord damage, suggesting infarction from direct compression of the cord or its arterial blood supply.
  • Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels

    Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels

    Elmer Press Original Article J Neurol Res • 2013;3(5):135-141 Level Diagnosis of Cervical Compressive Myelopathy: Signs, Symptoms, and Lesions Levels Naoki Kasahata ficult to accurately localize the lesion before radiographic Abstract diagnosis. However, neurological level diagnosis of spinal cord is important for accurate lesion-specific level diagnosis, Background: To elucidate signs and symptoms corresponding to patients’ treatment, avoiding diagnostic error, differential di- each vertebral level for level-specific diagnoses. agnosis, and especially for accurate level diagnosis of other nonsurgical myelopathies. Moreover, level diagnosis should Methods: We studied 106 patients with cervical compressive my- be considered from multiple viewpoints. Therefore, we in- elopathy. Patients who showed a single compressive site on mag- tend to make level diagnosis of myelopathy more accurate. netic resonance imaging (MRI) were selected, and signs, symp- Previously, lesion-specific level diagnoses by determin- toms, and the levels of the MRI lesions were studied. ing a sensory disturbance area or location of numbness in Results: Five of 12 patients (41.7%) with C4-5 intervertebral level the hands had the highest accuracy [1, 2]. Previous stud- lesions showed decreased or absent biceps and brachioradialis re- ies reported that C3-4 intervertebral level lesions showed flexes, while 4 of these patients (33.3%) showed generalized hyper- increased or decreased biceps reflexes, deltoid weakness, reflexia. In comparison, 5 of 24 patients (20.8%) with C5-6 inter- and sensory disturbance of arms or forearms [1, 3, 4], while vertebral level lesions showed decreased or absent triceps reflexes; C4-5 intervertebral level lesions showed decreased biceps however, 9 of these patients (37.5%) showed decreased or absent reflexes, biceps weakness, and sensory disturbance of hands biceps and brachioradialis reflexes.
  • Treating Dysosmia, from Saline to Surgery

    Treating Dysosmia, from Saline to Surgery

    日鼻誌４７!：５１～５２，２００８ 特別講演２ TREATING DYSOSMIA, FROM SALINE TO SURGERY Donald A. Leopold, MD, FACS University of Nebraska Medical Center, Omaha, Nebraska, United States of America The sense of smell begins with airflow through the nose. The exact path of this airflow has only recently been investigated. Some of this data comes from models, both life size and enlarged models using measurements of airflow. Additional information comes from computerized airflow models of the nasal cavities. The neural pathways of olfaction begin with the olfactory receptors high in the nasal cavity. After transduction from the chemical to the electrical information, this information is transferred through the olfactory bulb and into the central brain. Patients typically present with one of three different types of dysosmia. The first is simply a decreased ability to perceive smells（hyposmia and anosmia）. The two remaining types of dysosmia relate to distortions of perceived smells. One of these（parosmia）is a distortion of smell odorants that are actually in the environment. The third type is theperceptionofanodorwhenthereisnoodorantintheenvironment（phantosmia or hallucination）. The clinical task of the physician seeing these patients is to decide on the etiology of the problem and to recom- mend therapy if possible. The clinical history is one of the best tools the clinician has, but the physical examination, sensory testing and imaging can also be helpful. Diagnostic categories for these patients are many, but the most com- mon include nasal inflammatory disease for about a third of these patients, the losses that occur after an upper respira- tory infection in about 25 percent of the patients and head trauma in about 15 percent of patients.
  • Cerebellar Ataxia

    Cerebellar Ataxia

    CEREBELLAR ATAXIA Dr. Waqar Saeed Ziauddin Medical University, Karachi, Pakistan What is Ataxia? ■ Derived from a Greek word, ‘A’ : not, ‘Taxis’ : orderly Ataxia is defined as an inability to maintain normal posture and smoothness of movement. Types of Ataxia ■ Cerebellar Ataxia ■ Sensory Ataxia ■ Vestibular Ataxia Cerebellar Ataxia Cerebrocerebellum Spinocerebellum Vestibulocerebellum Vermis Planning and Equilibrium balance Posture, limb and initiating and posture eye movements movements Limb position, touch and pressure sensation Limb ataxia, Eye movement dysdiadochokinesia, disorders, Truncal and gait Dysmetria dysarthria nystagmus, VOR, ataxia hypotonia postural and gait. Gait ataxia Types of Cerebellar Ataxia • Vascular Acute Ataxia • Medications and toxins • Infectious etiologies • Atypical Infectious agents • Autoimmune disorders • Primary or metastatic tumors Subacute Ataxia • Paraneoplastic cerebellar degeneration • Alcohol abuse and Vitamin deficiencies • Systemic disorders • Autosomal Dominant Chronic • Autosomal recessive Progressive • X linked ataxias • Mitochondrial • Sporadic neurodegenerative diseases Vascular Ataxia ▪ Benedikt Syndrome It is a rare form of posterior circulation stroke of the brain. A lesion within the tegmentum of the midbrain can produce Benedikt Syndrome. Disease is characterized by ipsilateral third nerve palsy with contralateral hemitremor. Superior cerebellar peduncle and/or red nucleus damage in Benedikt Syndrome can further lead in to contralateral cerebellar hemiataxia. ▪ Wallenberg Syndrome In
  • Pearls: Infectious Diseases

    Pearls: Infectious Diseases

    Pearls: Infectious Diseases Karen L. Roos, M.D.1 ABSTRACT Neurologists have a great deal of knowledge of the classic signs of central nervous system infectious diseases. After years of taking care of patients with infectious diseases, several symptoms, signs, and cerebrospinal fluid abnormalities have been identified that are helpful time and time again in determining the etiological agent. These lessons, learned at the bedside, are reviewed in this article. KEYWORDS: Herpes simplex virus, Lyme disease, meningitis, viral encephalitis CLINICAL MANIFESTATIONS does not have an altered level of consciousness, sei- zures, or focal neurologic deficits. Although the ‘‘classic triad’’ of bacterial meningitis is The rash of a viral exanthema typically involves the fever, headache, and nuchal rigidity, vomiting is a face and chest first then spreads to the arms and legs. common early symptom. Suspect bacterial meningitis This can be an important clue in the patient with in the patient with fever, headache, lethargy, and headache, fever, and stiff neck that the meningitis is vomiting (without diarrhea). Patients may also com- due to echovirus or coxsackievirus. plain of photophobia. An altered level of conscious- Suspect tuberculous meningitis in the patient with ness that begins with lethargy and progresses to stupor either several weeks of headache, fever, and night during the emergency evaluation of the patient is sweats or a fulminant presentation with fever, altered characteristic of bacterial meningitis. mental status, and focal neurologic deficits. Fever (temperature 388C[100.48F]) is present in An Ixodes tick must be attached to the skin for at least 84% of adults with bacterial meningitis and in 80 to 24 hours to transmit infection with the spirochete 1–3 94% of children with bacterial meningitis.
  • PDF Generated By

    PDF Generated By

    The Evolution of Language: Towards Gestural Hypotheses DIS/CONTINUITIES TORUŃ STUDIES IN LANGUAGE, LITERATURE AND CULTURE Edited by Mirosława Buchholtz Advisory Board Leszek Berezowski (Wrocław University) Annick Duperray (University of Provence) Dorota Guttfeld (Nicolaus Copernicus University) Grzegorz Koneczniak (Nicolaus Copernicus University) Piotr Skrzypczak (Nicolaus Copernicus University) Jordan Zlatev (Lund University) Vol. 20 DIS/CONTINUITIES Przemysław ywiczy ski / Sławomir Wacewicz TORUŃ STUDIES IN LANGUAGE, LITERATURE AND CULTURE Ż ń Edited by Mirosława Buchholtz Advisory Board Leszek Berezowski (Wrocław University) Annick Duperray (University of Provence) Dorota Guttfeld (Nicolaus Copernicus University) Grzegorz Koneczniak (Nicolaus Copernicus University) The Evolution of Language: Piotr Skrzypczak (Nicolaus Copernicus University) Jordan Zlatev (Lund University) Towards Gestural Hypotheses Vol. 20 Bibliographic Information published by the Deutsche Nationalbibliothek The Deutsche Nationalbibliothek lists this publication in the Deutsche Nationalbibliografie; detailed bibliographic data is available in the internet at http://dnb.d-nb.de. The translation, publication and editing of this book was financed by a grant from the Polish Ministry of Science and Higher Education of the Republic of Poland within the programme Uniwersalia 2.1 (ID: 347247, Reg. no. 21H 16 0049 84) as a part of the National Programme for the Development of the Humanities. This publication reflects the views only of the authors, and the Ministry cannot be held responsible for any use which may be made of the information contained therein. Translators: Marek Placi ski, Monika Boruta Supervision and proofreading: John Kearns Cover illustration: © ńMateusz Pawlik Printed by CPI books GmbH, Leck ISSN 2193-4207 ISBN 978-3-631-79022-9 (Print) E-ISBN 978-3-631-79393-0 (E-PDF) E-ISBN 978-3-631-79394-7 (EPUB) E-ISBN 978-3-631-79395-4 (MOBI) DOI 10.3726/b15805 Open Access: This work is licensed under a Creative Commons Attribution Non Commercial No Derivatives 4.0 unported license.
  • Acquired Aphasia in Children

    Acquired Aphasia in Children

    13 Acquired Aphasia in Children DOROTHY M. ARAM Introduction Children versus Adults Language disruptions secondary to acquired central nervous system (CNS) lesions differ between children and adults in multiple respects. Chief among these differences are the developmental stage of language ac- quisition at the time of insult and the developmental stage of the CNS. In adult aphasia premorbid mastery of language is assumed, at least to the level of the aphasic's intellectual ability and educational opportunities. Acquired aphasia sustained in childhood, however, interferes with the de- velopmental process of language learning and disrupts those aspects of language already mastered. The investigator and clinician thus are faced with sorting which aspects of language have been lost or impaired from those yet to emerge, potentially in an altered manner. Complicating re- search and clinical practice in this area is the need to account continually for the developmental stage of that aspect of language under consideration for each child. In research, stage-appropriate language tasks must be se- lected, and comparison must be made to peers of comparable age and lan- guage stage. Also, appropriate controls common in adult studies, such as social class and gender, are critical. These requirements present no small challenge, as most studies involve a wide age range of children and ado- lescents. In clinical practice, the question is whether assessment tools used for developmental language disorders should be used or whether adult aphasia batteries should be adapted for children. The answer typically de- pends on the age of the child and the availability of age- and stage-appro- 451 ACQUIRED APHASIA, THIRD EDITION Copyright 1998 by Academic Press.
  • Taste and Smell Disorders in Clinical Neurology

    Taste and Smell Disorders in Clinical Neurology

    TASTE AND SMELL DISORDERS IN CLINICAL NEUROLOGY OUTLINE A. Anatomy and Physiology of the Taste and Smell System B. Quantifying Chemosensory Disturbances C. Common Neurological and Medical Disorders causing Primary Smell Impairment with Secondary Loss of Food Flavors a. Post Traumatic Anosmia b. Medications (prescribed & over the counter) c. Alcohol Abuse d. Neurodegenerative Disorders e. Multiple Sclerosis f. Migraine g. Chronic Medical Disorders (liver and kidney disease, thyroid deficiency, Diabetes). D. Common Neurological and Medical Disorders Causing a Primary Taste disorder with usually Normal Olfactory Function. a. Medications (prescribed and over the counter), b. Toxins (smoking and Radiation Treatments) c. Chronic medical Disorders ( Liver and Kidney Disease, Hypothyroidism, GERD, Diabetes,) d. Neurological Disorders( Bell’s Palsy, Stroke, MS,) e. Intubation during an emergency or for general anesthesia. E. Abnormal Smells and Tastes (Dysosmia and Dysgeusia): Diagnosis and Treatment F. Morbidity of Smell and Taste Impairment. G. Treatment of Smell and Taste Impairment (Education, Counseling ,Changes in Food Preparation) H. Role of Smell Testing in the Diagnosis of Neurodegenerative Disorders 1 BACKGROUND Disorders of taste and smell play a very important role in many neurological conditions such as; head trauma, facial and trigeminal nerve impairment, and many neurodegenerative disorders such as Alzheimer’s, Parkinson Disorders, Lewy Body Disease and Frontal Temporal Dementia. Impaired smell and taste impairs quality of life such as loss of food enjoyment, weight loss or weight gain, decreased appetite and safety concerns such as inability to smell smoke, gas, spoiled food and one’s body odor. Dysosmia and Dysgeusia are very unpleasant disorders that often accompany smell and taste impairments.
  • Neurovascular Anatomy (1): Anterior Circulation Anatomy

    Neurovascular Anatomy (1): Anterior Circulation Anatomy

    Neurovascular Anatomy (1): Anterior Circulation Anatomy Natthapon Rattanathamsakul, MD. December 14th, 2017 Contents: Neurovascular Anatomy Arterial supply of the brain . Anterior circulation . Posterior circulation Arterial supply of the spinal cord Venous system of the brain Neurovascular Anatomy (1): Anatomy of the Anterior Circulation Carotid artery system Ophthalmic artery Arterial circle of Willis Arterial territories of the cerebrum Cerebral Vasculature • Anterior circulation: Internal carotid artery • Posterior circulation: Vertebrobasilar system • All originates at the arch of aorta Flemming KD, Jones LK. Mayo Clinic neurology board review: Basic science and psychiatry for initial certification. 2015 Common Carotid Artery • Carotid bifurcation at the level of C3-4 vertebra or superior border of thyroid cartilage External carotid artery Supply the head & neck, except for the brain the eyes Internal carotid artery • Supply the brain the eyes • Enter the skull via the carotid canal Netter FH. Atlas of human anatomy, 6th ed. 2014 Angiographic Correlation Uflacker R. Atlas of vascular anatomy: an angiographic approach, 2007 External Carotid Artery External carotid artery • Superior thyroid artery • Lingual artery • Facial artery • Ascending pharyngeal artery • Posterior auricular artery • Occipital artery • Maxillary artery • Superficial temporal artery • Middle meningeal artery – epidural hemorrhage Netter FH. Atlas of human anatomy, 6th ed. 2014 Middle meningeal artery Epidural hematoma http://www.jrlawfirm.com/library/subdural-epidural-hematoma
  • Conduction Aphasia, Sensory-Motor Integration, and Phonological Short-Term Memory – an Aggregate Analysis of Lesion and Fmri Data ⇑ Bradley R

    Conduction Aphasia, Sensory-Motor Integration, and Phonological Short-Term Memory – an Aggregate Analysis of Lesion and Fmri Data ⇑ Bradley R

    Brain & Language 119 (2011) 119–128 Contents lists available at ScienceDirect Brain & Language journal homepage: www.elsevier.com/locate/b&l Conduction aphasia, sensory-motor integration, and phonological short-term memory – An aggregate analysis of lesion and fMRI data ⇑ Bradley R. Buchsbaum a, , Juliana Baldo b, Kayoko Okada d, Karen F. Berman e, Nina Dronkers b, ⇑ Mark D’Esposito c, Gregory Hickok d, a Rotman Research Institute, Toronto, Ontario, Canada b VA Northern California Health Care System, Center for Aphasia and Related Disorders, Martinez, CA, USA c Department of Psychology, University of California, Berkeley, CA, USA d Department of Cognitive Sciences, University of California, Irvine, CA, USA e Section on Integrative Neuroimaging, National Institute of Mental Health, Bethesda, MD, USA article info abstract Article history: Conduction aphasia is a language disorder characterized by frequent speech errors, impaired verbatim Accepted 11 December 2010 repetition, a deficit in phonological short-term memory, and naming difficulties in the presence of other- Available online 21 January 2011 wise fluent and grammatical speech output. While traditional models of conduction aphasia have typi- cally implicated white matter pathways, recent advances in lesions reconstruction methodology Keywords: applied to groups of patients have implicated left temporoparietal zones. Parallel work using functional Conduction aphasia magnetic resonance imaging (fMRI) has pinpointed a region in the posterior most portion of the left pla- Working memory num temporale, area Spt, which is critical for phonological working memory. Here we show that the Speech production region of maximal lesion overlap in a sample of 14 patients with conduction aphasia perfectly circum- Planum temporale Brain lesion scribes area Spt, as defined in an aggregate fMRI analysis of 105 subjects performing a phonological work- Sensorimotor integration ing memory task.
  • Loss of Taste and Smell After Brain Injury

    Loss of Taste and Smell After Brain Injury

    Loss of taste and smell after brain injury Introduction Following a brain injury many people report that their senses of taste and/or smell have been affected. This may be as a consequence of injury to the nasal passages, damage to the nerves in the nose and mouth, or to areas of the brain itself. Loss or changes to smell and taste are particularly common after severe brain injury or stroke and, if the effects are due to damage to the brain itself, recovery is rare. The effects are also often reported after minor head injuries and recovery in these cases is more common. If recovery does occur, it is usually within a few months of the injury and recovery after more than two years is rare. Sadly, there are no treatments available for loss of taste and smell, so this factsheet is designed to provide practical suggestions on how you can compensate. It provides information on health, safety and hygiene issues, suggestions to help you to maintain a healthy, balanced diet, information on psychological effects and some other issues to consider. How are taste and smell affected by brain injury? The two senses can both be affected in a number of different ways and some definitions of the terms for the different conditions are provided below: Disorders of smell Anosmia Total loss of sense of smell Hyposmia Partial loss of sense of smell Hyperosmia Enhanced sensitivity to odours Phantosmia/Parosmia ‘False’ smells – Perceiving smells that aren’t there Dysosmia Distortion in odour perception Disorders of taste Dysgeusia Distortion or decrease in the sense of taste Ageusia Total loss of sense of taste Dysgensia Persistent abnormal taste Parageusia Perceiving a bad taste in the mouth 1 The two senses are connected and much of the sensation of taste is due to smell, so if the sense of smell is lost then the ability to detect flavour will be greatly affected.
  • Correlation of CT Cerebral Vascular Territories with Function: 3. Middle Cerebral Artery

    Correlation of CT Cerebral Vascular Territories with Function: 3. Middle Cerebral Artery

    161 Correlation of CT Cerebral Vascular Territories with Function: 3. Middle Cerebral Artery Stephen A. Berman 1 Schematic displays are presented of the cerebral territories supplied by branches of L. Anne Hayman2 the middle cerebral artery as they would appear on axial and coronal computed Vincent C. Hinck 1 tomographic (CT) scan sections. Companion diagrams of regional cortical function and a discussion of the fiber tracts are provided to simplify correlation of clinical deficits with coronal and axial CT abnormalities. This report is the third in a series designed to correlate cerebral vascular territories and functional anatomy in a form directly applicable to computed tomog­ raphy (CT). The illustrations are intended to simplify analysis of CT images in terms of clinical signs and symptoms and vascular territories in everyday practice. The anterior and posterior cerebral arteries have been described [1 , 2] . This report deals with the middle cerebral arterial territory. Knowledge of cerebral vascular territories can help in differentiating between infarction and other pathologic processes. For example, if the position and extent of a lesion and the usual position and extent of a vascular territory are incongruous, infarction should receive relatively low diagnostic priority and vice versa. Knowledge of vascular territories can also facilitate correct interpretation of cerebral angio­ grams by pinpointing specific vessels for particularly close attention. Knowledge of functional neuroanatomy applied to a patient's clinical findings can improve detection of subtle lesions by pinpointing specific areas for special attention on CT and specific vessels for attention on angiograms. Discussion The largest area of the brain that is normally supplied by the vessel(s) of the middle cerebral territory is indicated in figures 1 and 2.