History of stroke

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Slide 1 : History of Cerebrovascular Disease Where have we been? Where are we now? Where should we go in the future?
Slide 2 : “The past is always with us, never to be escaped; it alone is enduring; but amidst the changes and chances which succeed one another so rapidly in this life, we are apt to live too much for the present and too much in the future.” Sir William Osler, Aequanimitas, 1889
Slide 3 : “We cannot afford to repeat the history of neurology every two decades” C Miller Fisher
Slide 4 : Sir William Osler (1849-1919) Bacterial Endocarditis and Rheumatic Heart Disease and Brain Embolism-1900
Slide 5 : 400 BC-1700 AD Emphasis on Prognosis and early Exploration of Brain Anatomy and Function Hippocrates- circa 400 BC Galen 130-200 AD Andre Vesalius 1514-1564 Johann Wepfer 1620-1695 Sir Thomas Willis 1621-1675 The Past
Slide 6 : Andreas Vesalius 1514-1564 De Humani Corpis Fabrica (1543) Woodcuts and copper plates created by an artist (Jan Kalkar) from dissections of humans made by Vesalius The 7th book of the Fabrica contains 15 drawings of the Brain based on dissections The Past-Anatomy
Slide 7 : Johann Jakob Wepfer 1620-1695 Observationes Anatomicae, ex Cadaveribus Eorum, quos Sustulit Apoplexia (1658) Performed necropsies and showed that bleeding into the brain was an important cause of apoplexy Described the anatomy and presence of hardening and occlusions within the intracranial Carotid and Middle Cerebral Arteries The Past-Pathology
Slide 8 : Sir Thomas Willis 1621-1675 Dissections described and illustrated by Sir Christopher Wrenn in Cerebri Anatomi (1664) Clarified anatomy of the Brain and Cranial Nerves Dissected cranial arteries and described connections at the base of the Brain (Circle of Willis) Respected clinician who described TIAs and Migraine The Past- Anatomy and Clinical
Slide 9 : Sir Thomas Willis Sedleian Professor of Natural Philosophy at Oxford University
Slide 10 : Sir Thomas Willis Robert Hooke (physicist) Robert Boyle (physicist) Richard Lower (anatomist and dissector) Sir Christopher Wrenn Sir Thomas Millington (physician) consultants and collaborators- William Harvey, John Locke, Sir Isaac Newton King and Lower administered the first recorded blood transfusion
Slide 11 :
Slide 12 :
Slide 13 : Diagram of an Anastamosis - Willis 1664
Slide 14 : Sir Thomas Willis -- TIA “ the irradiation of the spirits is wont to be interupted with little clouds, as it were, scatterred here and there but in the former, the same is forthwith wholly darkened and undergoes total eclipse.” Instructions and prescripts for curing the apoplexy- in Pordage S (Ed) The London Practice of Physic, 1679
Slide 15 : 1800-1925 Emphasis on Pathology and Disease Giovanni Battista Morgagni (1682-1771) John Cheyne (1777-1836) Richard Bright (1759-1858) Rudolph Virchow (1821-1902) Sir William Osler (1849-1919) The Past
Slide 16 : Giovanni Battista Morgagni1682-1771 De Sedibus et Causis Morborum per Anatomen Indagatis (The seats and causes of disease investigated by anatomy) 1769 published at age 79 De Sedibus - 5 Volumes containing 70 letters to a young man describing symptoms during life and pathology First Volume is Disease of the Head and begins with Apoplexy The Past- clinical-path correlations
Slide 17 : Giovanni Battista Morgagni “A certain man, a native of Genoa, blind of one eye, and lived by begging, being drunk and quarreling with othe3r drunken beggars received two blows by their sticks- one slight on the hand and another violent one at the left temple so that blood came out of the left ear. Yet soon after the quarrel became made up, he sat down at the fire with them…and again filled himself with a great quantity of wine by way of pledge of friendship being renewed. Not long after, on the same night, he died” Necropsy showed a large epidural hematoma. Morgagni also described cases of intracerebral hemorrhage and recognized that paralysis often involved the limbs on the opposite side of the hemorrhage.
Slide 18 : Giovanni Battista Morgagni Commenting on a diseased artery: “I opened both these arteries and on their internal surfaces I found a little white body, thickish, somewhat hard and even almost cartilaginous; it could not but happen that they must in some measure stop up the cavity as they protruded internally.”
Slide 19 : John Cheyne 1777-1836 Cases of Apoplexy and Lethargy with Observations upon the Comatose Diseases -1812 Separated Lethargy and Coma from Apoplexy Separated Brain softenings from ICH and SAH Sanguinous Apoplexies much more common than Serous Apoplexies The Past-Pathology
Slide 20 : 1812
Slide 21 : Rudolph Ludwig Carl Virchow (1821-1902) Clearly showed that vascular occlusion caused infarction Described the phenomenology of arterial thrombosis Recognized the important interaction between the vascular wall and the blood Described embolism The Past-Pathology & pathophysiology
Slide 22 : Rudolph Ludwig Carl Virchow
Slide 23 : Rudolph Ludwig Carl Virchow Virchow analyzed the relationship between thrombi and infarction, locally and at a distance. Among 76 necropsies performed in 1847, Virchow found thrombi in the veins of the extremities in 18 patients and within the pulmonary arteries in 11. Virchow reasoned that the bloodstream emanating from these veins must have been the conduit for transportation of these thrombi to distant sites like the lung arteries. He then used animal experiments to study the fate of foreign materials placed in the veins . Virchow then sought and found obstruction of brain, splenic, renal, and limb arteries at necropsy in patients who had cardiac valve disease and left atrial thrombi. Virchow thus systematically proved that in-situ thrombosis and embolism were the cause of infarction and that the process was not dependent on inflammation.
Slide 24 : Virchow and his Triad Virchow was the first to conclusively show that occlusion of arteries caused infarction He emphasized 3 components of vascular occlusion Circulatory stasis Endothelial injury Increased coagulability of the blood
Slide 25 : First awakening of Interest in phenomenology and their anatomical explanations 1810 Publication of The case of Dr Gaspard Vieusseux after his presentation to the Medical and Chirurgical Society of London. The author was Marcet, the secretary of the Society
Slide 26 :
Slide 27 : Vieusseux -1810 Dec 29, 1807 Vieusseux developed an unusual and severe pain in the left gum and jaw. 5 days later the pain recurred along with severe pain in the left eye. He then developed severe vertigo. “A peculiar and inexpressible perturbation in all his sensations” a giddiness that affected his vision and “occasioned feelings similar to those produced by a ship violently agitated.” He then lost his voice, had difficulty swallowing, and felt that his left side was weak.
Slide 28 : Vieusseux -1810 He then examined himself and found that “the whole of his right side was so insensible that he could be scratched or pinched without experiencing any pain and that this insensibility abruptly terminated at a line dividing the whole body in a vertical direction” The sensations of heat and cold were totally different from normal on his right side but he was puzzled to find that he had not lost the perception of touch on his right side. The left side of the head and face were also insensible to pricking or scratching over the left forehead, nose, lips, chin, and ear.
Slide 29 : Vieusseux -1810 The whole of the left side of the body preserved its usual degree of sensibility.” He also noted that his left eye was partially shut and the left corner of the mouth was drawn downward. His left leg dragged when he walked. During the next weeks the dysarthria and dysphagia improved but he developed hiccups “His intellectual faculties remained quite unimpaired so that he could accurately observe the whole succession of symptoms.”
Slide 30 : 1850-1950 - Focus on Vascular Anatomy and Clinical- Anatomical correlations. How the Brain works as seen from Vascular cases. Duret, Stopford, Gillilan, Duvorny Weber, Benedikt, Claude, Millard, Gubler, Babinski, Nageotte, Foville Wallenberg Jules Dejerine Charles Foix The Past-clinical-anatomic correlations
Slide 31 : Adolph Wallenberg (1862-1949)
Slide 32 : Wallenberg A. Anatomischer befund in einem als akute bulbaraffection (Embolie der arteria cerebelli inferior posterior sinistra) beschreibenen falle. Arch Psychiatrie 1901
Slide 33 :
Slide 34 : Joseph Jules Dejerine 1849-1917 Anatomie des Centres Nerveux (with Augusta Klumpke)1895-1901 Semiologie des Affections du Systeme Nerveux -1914 Master of Clinico-Anatomical correlations The Past
Slide 35 : Joseph Jules Dejerine
Slide 36 :
Slide 37 : 1895-1901
Slide 38 : 1914
Slide 39 : Central Facial Palsy
Slide 40 : Hemi-Medullary Infarct Bilateral Medial Medullary Infarct
Slide 41 : Alexia without Agraphia
Slide 42 : Alexia without Agraphia
Slide 43 : Charles Foix (1882-1927) During a 3 year period 1924-1927 Foix and colleagues defined the blood supply, location of “ramollissements”, and clinical symptoms and signs: Middle Cerebral Artery Anterior Cerebral Artery Anterior Choroidal Artery Posterior Cerebral Artery Thalamus Pons Lateral Medulla
Slide 44 : Charles Foix The Past
Slide 45 : Charles Foix
Slide 46 :
Slide 47 : MCA dissections
Slide 48 :
Slide 49 :
Slide 50 :
Slide 51 : Foix- Syndromes of the MCA- 1927 Ramollissement sylvien total Grand ramollissement sylvien profond Ramollissement partiels du territoire profond Grand ramollissement sylvien superficial Ramollissement partiels du territoire posterieure Ramollissement partiels rolandique et anterieurs Ramollissement multiples, bilateral et associes
Slide 52 : Foix- Syndromes of the MCA- 1927 Rules for distinguishing deep vs superficial MCA territory lesions Favoring deep lesions are: L’absence d’hemianopsie L’absence relative de troubles sensitifs Le caractere relativement proportionel de l’hemiplegie L’attente simultanee des deux membres Peut-etre y a-t-il aussi un argument a tirer du caractere franchement distal de la paralysie
Slide 53 : Foix & Schiff-Wertheimer1926 Revue d’Oto- neuro-oculistique4:561-584. Visual Radiations and their Arterial Supply
Slide 54 :
Slide 55 : Ramollissement Protuberentiels Foix et Hillemand 1926 Syndrome du territoire paramedian: Le tableau clinique en est simple: le malade presente comme un hemiplegie banal Syndrome du territoire des circumferential courtes: les signes cerebelleux siegent de la cote de la lesion alors que les signes pyramidaux et sensitif tres discrets peuvent manquer ou siegent du cote oppose a la lesion
Slide 56 : 1927-1975- Interest in the Pathology and Pathophysiology of Vascular lesions Charles Foix 1927. Arteries leading to ‘ramolissements” were often not occluded Raymond Adams and Charles Kubik- 1946- Basilar Artery occlusion C Miller Fisher 1951-present Pathology, pathophysiology and clinical correlations of : ICA disease, brain hemorrhage, vertebro-basilar disease, lacunes
Slide 57 :
Slide 58 : Foix, Hillemand, Levy. Relativement au ramollissement cerebral a sa frequence et a son siege a l’importance relative des obliterations arterielles, completes ou incompletes dans sa pathogenie. Rev Neurol 1927 (abstract) L’obliteration etait totale dans 12 cas/56 Subtotal dans 14 cas Et dans 30 cas elle lassait un calibre permeable assez important Obliteration complete apres du ramollissement Embolies Du territoire insufficance cardio-arteriel Un spasme arteriel
Slide 59 : Raymond D Adams
Slide 60 : 1946
Slide 61 : Occlusion of the Basilar Artery, Brain 1946
Slide 62 : Charles Miller Fisher Pathology and Clinical Features of ICH (1961-71) Clinical features (1951-4) and pathology (1986) of Carotid Artery Disease Clinical features of Vertebral artery disease (1971) and Vascular lesions in Lateral Medullary Infarcts (1961) Clinical and pathological features of Lacunar infarction (1965-present)
Slide 63 : Charles Miller Fisher
Slide 64 :
Slide 65 :
Slide 66 : 1961
Slide 67 : 1971
Slide 68 : Fibrin globes
Slide 69 : 1971
Slide 70 : 1951
Slide 71 : Fisher, Karnes, Kubik. Lateral Medullary Infarction. The pattern of vascular occlusion. J Neuropath Exp Neurol 1961
Slide 72 : Fisher, Caplan. Basilar Artery Branch Occlusion. Neurology 1971.
Slide 73 : 1977 Bilateral Basilar branch disease
Slide 74 : Derek Denny-Brown
Slide 75 : Recurrent Cerebrovascular EpsisodesDenny-Brown, Arch Neurology 1960 “We therefore postulate an explanation alternative to vasospasm, namely a state of carotid insufficiency, determined by either stenosis or occlusion of the internal carotid artery with its vascular territory left supplied by collateral branches. A similar situation in relation to the basilar artery accounts for insufficiency of supply to the brainstem and posterior cerebral territory of that artery. Carotid or basilar insufficiency is a physiological, potentially hemodynamic state in which reversible hemodynamic crises could be elicited by any factor that impaired collateral circulation.”
Slide 76 : 1978-Present - Stroke Data Banks and Registries Dalsgaard-Nielsen -1955 Mayo Clinic - 1945-1954 ;1955-1969 Harvard Stroke Registry -1978 Stroke Data Bank -1988 Lausanne Stroke Registry 1988-present German Stroke Data Bank 2001-present The Past
Slide 77 : 1970-2005 Focus on Technology development, Treatment especially acute, Epidemiology, and Evidence-based Medicine in a Managed Care environment The Present
Slide 78 : 1970-2005 Technology is rapidly improving and still developing. CT and MRI allow delineation of the location and type of lesion and CTA and CT perfusion, MRA, and extracranial and transcranial ultrasound (TCD) allow definition of arterial lesions. Echocardiography, cardiac rhythm monitoring, and blood analysis detect cardiac, aortic, and hematological causes of stroke. Neurologists of today can quickly and safely define the cause and extent of cerebrovascular disease. The Present
Slide 79 : 1970-2005 Epidemiological studies worldwide define stroke risk factors and factors related to outcomes and differences in stroke subtypes, stroke risk factors, and vascular lesions according to age, race, and sex The Present
Slide 80 : 1970-2005 This is the era of therapy. The introduction of thrombolysis and endovascular treatments focus attention on rapid delivery and throughput of patients. Randomized therapeutic trials are considered essential to provide a true evidence-base for treatment of stroke patients. Statisticians are kings. Managed Care directors and Insurers control the purse strings. The Present
Slide 81 : 2005- ? Genetics More Stroke-ICU Specialists and Hospitalists More Endovascular devices and treatments Stem Cell Therapies More technology-based definition of the cause of strokes in individual patients Focus more on Recovery and Rehabilitation The Future
Slide 82 : 2005-? - Genetics Use of genetic information will proliferate. Physicians will be able to study individual patient’s genetic make-up to predict risks and take measures to reduce those risks. Study of the genetics of vascular disease will identify new treatment strategies. Endovascular introduction of genetic materials and stem cells may play an important role in treatment. The Future
Slide 83 : 2005-? Upgrade in Hospital Care for Stroke patients Accredited Stroke Centers at various levels More Stroke-ICU trained Neurologist specialists More Hospitalists for Stroke The Future

 


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