SEARCH RESULTS FOR: Aphasia

Aphasia

Aphasia (Wernicke’s and Broca’s): Pathogenesis and clinical findings Authors: Davis Maclean Reviewers: Heather Yong Tony Gu Yan Yu* Scott Jarvis* *MD at time of publication Ischemic stroke (common) Local Invasion (e.g. by a tumour, Head infection, or hemorrhage) Trauma Intracerebral Hemorrhage Dementia (e.g. Fronto- temporal Dementia) Episodic occurrences (e.g., migraine, epilepsy) Damage to language-dominant cerebral hemisphere (the left hemisphere, for the majority of humans): Damage affecting Broca’s Area in the Inferior frontal gyrus (area 44 & 45) Damage affecting Wernicke’s Area in the posterior part of the superior temporal gyrus (area 22) Localization: Inferior frontal gyrus, superior sylvian fissure Blood supply: superior division M2 branch middle cerebral artery Localization: Posterior perisylvian region, temporal lobe Blood supply: inferior division M2 middle cerebral artery Sensory speech areas still intact (posterior superior temporal lobe) Intact comprehension (intact hearing & reading) Impaired function of Broca’s Area ↓ output or generation of speech/ text If function of nearby motor areas is also impaired Contralateral hemiparesis (face, arm > leg) If function of other nearby areas is also impaired Impaired naming and repetition Motor speech areas still intact (inferior frontal lobe) Fluent (but non-sensical) speech output Impaired function of Wernicke’s Area Impaired compre- hension (i.e. cannot understand speech or text) Loss of sensory speech input to motor areas Errors in word usage, tense, structure If function of nearby sensory areas is impaired Contralateral sensory deficits Broca’s Aphasia Wernicke's Aphasia (Expressive language impairment: non-Fluent) Notes/Definitions: (Receptive language impairment/Fluent: the person can talk but their speech is nonsensical) • Dysarthria ≠ Aphasia (Dysarthria: disruption to neurons controlling the muscles that produce sounds, resulting in slurred/disjointed speech. Aphasia: acquired deficit in language comprehension or generation/output usually due to disruption of neurons in the cerebral cortex.) • “Global” aphasia affects both receptive and expressive language. Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 1, 2020 on www.thecalgaryguide.com

presentation-of-sah

Subarachnoid Hemorrhage: Clinical Findings Sudden bleeding into space surrounding the brain (for pathogenesis, see Subarachnoid Hemorrhage: Pathogenesis) Authors: Jason An, M. Patrick Pankow Reviewers: Owen Stechishin, Dave Nicholl, Haotian Wang, Hannah Mathew, Ran (Marissa) Zhang, Yan Yu*, Cory Toth* * MD at time of publication Bleed into subarachnoid space Subarachnoid Hemorrhage (SAH) Posterior hypothalamus ischemia (↓ Blood flow and oxygen) Red blood cell lysis from energy depletion or complement activation Release of spasmogens (spasm inducing agents) Cerebral vasospasm (narrowing of arteries from persistent contraction) ↓ blood flow Cerebral ischemia Release catecholamines (hormones from the adrenal gland; e.g., epinephrine, norepinephrine) ↑ Intracellular calcium Release of antidiuretic hormone Antidiuretic hormone acts on the distal convoluted tubule and collecting duct in kidney to reabsorb water Dilution of serum sodium Hyponatremia (low blood sodium levels) Release of epileptogenic (potential seizure causing agents) into cerebral circulation Seizure Products from blood breakdown in cerebral spinal fluid Irritation of meninges (membranes surrounding the brain) Aseptic meningitis (non-infectious inflammation) Meningismus (neck pain + rigidity) Cerebral infarction (death of tissue) Obstructs cerebral spinal fluid flow and absorption at subarachnoid granulations Hydrocephalus (fluid build up in ventricles) ↓ Level of consciousness Reduced cerebral blood flow Dilation of cranial vessels to ↑ blood flow Rapid ↑ internal carotid artery intracranial pressure Refer to Increased Intracranial Pressure: Clinical Findings slide Internal carotid artery Pituitary ischemia Hypopituitarism [underactive pituitary gland, failing to produce 1+ pituitary hormone(s)] Refer to hypopituitarism slides Myocardial disruption Left ventricle dysfunction ↑ Pressure in left heart Blood forced backwards into pulmonary veins ↑ Pulmonary blood pressure Fluid from blood vessels leaks into lungs Dysrhythmias (disturbance in rate/rhythm of heart) causing ↓ cardiac output Syncope (loss of consciousness due to ↓ blood flow to the brain) Pulmonary edema (excess accumulation of fluid in lung) Cerebral hypoperfusion Sudden ↑in blood volume Vessels and meninges suddenly stretch Thunderclap Headache (worst headache of patient's life) Shortness of breath Reactive cerebral hyperemia (excess blood in vessels supplying the brain) Artery specific findings: Rapid ↑ internal carotid artery intracranial pressure Middle cerebral artery Posterior communicating artery Compression of outer CN3 Compression of inner CN3 Anterior communicating artery Nonreactive pupil Gaze palsy (eye deviates down and out) Diplopia (double vision) Ptosis (drooping of upper eyelid) Frontal lobe ischemia Avolition (complete lack of motivation) Ischemia of motor strip pertaining to the legs Bilateral leg weakness Motor strip ischemia Hemiparesis (weakness/ inability to move one side of the body) Ischemia of parietal association areas (brain regions integral for motor control of the eyes, the extremities and spatial cognition) Aphasia (impaired ability to speak and/or understand language)/ neglect Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 1, 2014, updated August 10, 2022 on www.thecalgaryguide.com

Ischemic Stroke Impairment by Localization

Ischemic Stroke: Impairment by localization Contralateral weakness and sensory loss in the lower extremity Authors: Andrea Kuczynski Yvette Ysabel Yao Reviewers: Sina Marzoughi Usama Malik Mao Ding Andrew M Demchuk* * MD at time of publication Ischemia in the anterior cerebral artery Motor and sensory cortices of lower limb damage Hypertension, dyslipidemias, diabetes, smoking Atherosclerosis, thrombosis, or stenosis (narrowing) in respective blood vessels Ischemia: ↓ blood flow (See Ischemic Stroke: Pathogenesis slide) Left hemisphere damage Right hemisphere damage Motor and sensory cortices of upper limb and face damage Urinary incontinence Aphasia (inability to comprehend or produce Ischemia in the middle cerebral artery (MCA) MCA divides into segments language) (See Aphasia slide) Left sided agnosia (visual perceptual deficits) Contralateral hemiparesis (weakness on side of body opposite to injury) & sensory deficits, visual field deficits, aphasia, agnosia (inability to process sensory information), apraxia (motor planning deficits) & agraphia (inability to communicate by writing) M1-MCA (sphenoidal segment) M2-MCA (insular segment) Ischemia in the posterior cerebral artery Spares the lower extremity, affects the upper extremity and face Lesion to frontal lobe (Broca area) Infarction of occipital cortex Lesion to superior temporal gyrus of temporal lobe (Wernicke area) No homonymous hemianopsia (one-sided visual field loss) Expressive Broca’s/motor aphasia (inability to produce language) Contralateral homonymous hemianopsia (visual field loss on opposite side) Receptive Wernicke’s/sensory aphasia (inability to comprehend language) Sensory loss, memory loss, contralateral homonymous hemianopsia & alexia (reading difficulty) Ischemia of the occipital lobe, posteromedial temporal lobes, midbrain & thalamus Ischemia in the vertebral basilar artery Ischemia in the basilar artery Ischemia of brainstem & medulla Ischemia of midbrain, thalami, inferior temporal & occipital lobes Cranial nerve disorders: dysarthria (slurred/slowed speech) (IX, X), diplopia (double vision), facial numbness or paresthesia (VII), Foville’s syndrome (ipsilateral cerebellar ataxia), Horner's syndrome, (paresis of conjugate gaze and contralateral hemiparesis, facial palsy, pain & thermal hypoesthesia) Motor deficits: Millard-Gubler syndrome (pons lesion), Raymond’s syndrome (ipsilateral abducens impairment, contralateral central facial paresis & contralateral hemiparesis), Wallenburg syndrome (sensory deficits in the contralateral limb, ipsilateral face), ataxia (abnormal gait), unilateral or bilateral sensory loss of position & vibration Cranial nerve disorders: dysconjugate gaze (unpaired eye movements) (III, IV, VI), ipsilateral facial hypoalgesia (↓ pain sensitivity) (V), unilateral lower motor neuron face paralysis (VII), vertigo (spinning sensation), dysarthria (weak speech muscles) (IX, X) Motor deficits: contralateral hemiparesis, quadriplegia (paralysis of all 4 limbs), contralateral limb hypoalgesia Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications First published February 3, 2018, updated February 28, 2023 on www.thecalgaryguide.com

Hemorrhagic Stroke

Hemorrhagic Stroke: Pathogenesis and clinical findings Authors: Andrea Kuczynski Oswald Chen Reviewers: Sina Marzoughi Usama Malik Anjali Arora Ran (Marissa) Zhang Mao Ding Michael D Hill* Gary Klein* * MD at time of publication Primary Intracerebral Hemorrhage (~75%) Secondary Intracerebral Hemorrhage (~25%) Amyloid Angiopathy Amyloid deposits in blood vessels and weakens vessel walls Hypertension Lipohyalinosis (lipid and protein aggregation in arterial walls) weakens blood vessels Unknown Aneurysm Dilation of a weakened blood vessel Drugs (e.g., cocaine, crystal meth, decongestants, anticoagulants) Vascular Malformations Note: the pathophysiology and exact mechanism is not well known Release of toxic blood plasma components (coagulation factors, immunoglobins) Red blood cell lysis Cytotoxic hemoglobin (heme, iron) release Fenton-type free radical generation (Fe(II) + H2O2 → Fe(III) + OH− + OH•) Oxidative damage to carbohydrates, lipids, nucleic acids, and proteins in brain Necrosis of hypoxic brain tissue Neurological signs: focal motor weakness, aphasia, vision loss, sensory loss, imbalance/incoordination, altered LOC Rupture of blood vessel(s) Accumulation of blood → hematoma formation ↓ Cerebral tissue perfusion (↓ O2 availability) ↓ Mitochondrial oxidative phosphorylation (final step in aerobic glucose metabolism) ↓ Adenosine triphosphate (ATP) production ↑ Anaerobic glucose metabolism → ↑ Cerebral lactate production Cerebral lactic acidosis Impaired cellular metabolism Death of neurons and glia Microglia clear debris and release inflammatory markers (TNFα, IFγ, IL-1β) ↑ Endothelial cell apoptosis and ↑ blood-brain barrier permeability Cerebral edema Increased intracranial pressure: papilledema, sudden headache, non-reactive pupils, ↓ level of consciousness (LOC), nausea/vomiting Astrocytes release glutamate (main excitatory neurotransmitter) Activation of neuronal metabotropic glutamate receptors ↑ Ca2+ influx into neurons Excitotoxicity (excess stimulation of glutamate receptors leading to neuronal death) Dysfunction of Na+/K+ ATPase pump (moves 3 Na+ out of cell and 2 K+ into cell) on neurons ↓ Na+ efflux and ↓ K+ influx Neuronal membrane potential becomes less negative (closer to threshold potential) Neurons depolarize → ↑ Glutamate release General findings: Seizures, lethargy Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications First published June 6, 2018, updated February 28, 2023 on www.thecalgaryguide.com