SEARCH RESULTS FOR: intracerebral hemorrhage

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

chronic-hypertension-complications

Chronic Hypertension: Complications Chronic Hypertension Long term Blood Pressure (BP) ≥ 135/85 (on ambulatory or home blood pressure measurement) in patients without diabetes, or BP ≥ 130/80 in patients with diabetes Authors: Samin Dolatabadi, Yan Yu* Reviewers: Meena Assad, Jessica Krahn Juliya Hemmett* * MD at time of publication ↑ Afterloadà ↑ Resistance to left ventricle ejection To overcome resistance and preserve cardiac output, the myocardium undergoes structural and functional changes Left ventricular hypertrophy and fibrosis Stiff ventricle ↓ Contractility of the left ventricle Impaired forward flow of blood from heart Chronic stress on the endothelium of systemic blood vessels ↑ Blood pressure in retinal circulation Hypertensive Retinopathy (See slide on Chronic Hypertensive Retinopathy: Pathogenesis and Clinic Findings) Smooth muscle of kidney’s afferent arterioles constricts to prevent transmission of ↑ blood pressure to glomerulus Overtime, smooth muscles of afferent arterioles hypertrophy from prolonged vasoconstriction Chronic stress and trauma on endothelial and smooth muscle cells of kidney Injury leads to excretion of cytokines and extracellular matrix such as fibrin and collagen into subendothelial layer Endothelial dysfunction (See slide on Atherosclerosis: Pathogenesis) Atherosclerosis Loss of normal arterial architecture in the brain due to stress of ↑ blood pressure Weakening of cerebral arteries Formation and rupture of microaneurysms Intracerebral Hemorrhage Accumulation of plaques in the walls of cerebral arteries ↓ Cerebral blood flow Ischemic Stroke Accumulation of plaques in the walls of coronary arteries ↓ Myocardial blood flow Oxygen supply- demand mismatch Coronary Artery Disease Thickening of arteriolar wall and narrowing of afferent arterioles ↓ Glomerular blood flow Glomerular and tubular ischemia Glomerular sclerosis and tubular atrophy Blood backs up into lungs ↓ perfusion of blood throughout the bodyà inability of the heart to meet metabolic demands Congestive Heart Failure Hypertensive Nephrosclerosis Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published December 4, 2021 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

Epilepsy in Older Adults

Epilepsy in Older Adults: Pathogenesis and clinical findings Cerebrovascular disease (1⁄3 of cases), primarily ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage Ischemic and hemorrhagic injuries cause inflammation and nerve cell degeneration Glial cells (astrocytes and oligodendrocytes) proliferate around the lesion area to repair the damaged tissue Glial scar formation impedes neuronal reconnection and growth Alzheimer’s or Vascular Dementia Central nervous system disease (e.g. traumatic brain injury, prior meningitis, mass) Medications associated with hyponatremia (e.g. diuretics, antidepressants, antipsychotics, etc.) Cerebral edema Increased intracranial pressure Compression on structures and blood vessels Sleep deprivation Tau or amyloid deposition (abnormal protein aggregates in brain) Small vessel disease Increased delta wave activity Heightened neural excitability Decreased seizure threshold Elevated stress hormones (e.g. cortisol) Increased neuronal excitability and decreased inhibition Areas of tissue death, white matter changes & cortical irritability Structural and electrical brain changes Epilepsy: Neurological disorder characterized by increased susceptibility to recurrent unprovoked seizures Excessive, hypersynchronous & oscillatory network function Imbalance between excitatory and inhibitory activity Resultant seizure activity Atypical Seizure pattern; e.g. seem confused, stare into space, wander, make unusual movements, inability to answer questions Often atypical location in brain (limbic or neocortical) Focal seizures are more common than generalized Postictal paresis can last for days & disorientation, hyperactivity, wandering and incontinence may persist for 1 week Neurotransmitter dysregulation, neural network disruption, genetic factors, psychosocial factors Psychiatric comorbidities Authors: Anna Crone Reviewers: Anika Zaman, Rachel Carson, Raafi Ali, Luiza Radu, Gary Michael K Klein* * MD at time of publication Widespread structural changes and hippocampal atrophy Dementia Sub-optimal treatment results in ongoing and more frequent epileptic seizures Status epilepticus (higher mortality among older adults) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Oct 4, 2024 on www.thecalgaryguide.com