SEARCH RESULTS FOR: TINNITUS

Tinnitus

Vestibular Neuritis

Vestibular Neuritis: Pathogenesis and Clinical Findings Authors: Ryan Chan Jonathan Wong Reviewers: Mehul Gupta Davis Maclean Saud Sunba Yan Yu* Euna Hwang* * MD at time of publication Recent viral illness or upper respiratory tract infection Virus spreads along upper respiratory mucosa and into the inner ear structures Vestibular Neuritis Presumed idiopathic viral-induced inflammation of the vestibular nerve; typically unilateral Reactivation of Herpes Simplex Virus-1 in vestibular (Scarpa’s) ganglion Inflammatory cell infiltration leads to degeneration and atrophy of the vestibular nerve Superior Vestibular Neuritis (40-48%) Inflammatory cells traverse through only one long bony canal, easier for inflammatory cell infiltration Loss of afferent innervation from the superior and horizontal semicircular canal (SCC), utricle, and parts of the saccule Combined Superior Vestibular Neuritis and Inferior Vestibular Neuritis (34-56%) Inferior Vestibular Neuritis (1.3-18%) Inflammatory cells must pass through two separate bony canals, making inflammatory cell infiltration more difficult Loss of afferent innervation from the posterior semicircular canal (SCC) and saccule Utricular degeneration Displacement of otoliths/ otoconia (commonly into the posterior SCC) BPPV (can occur several months after onset of neuritis) Loss of horizontal SCC afferent neuron signaling to the brain Unilateral Loss or ↓ of normal nystagmus response to Caloric Testing (insertion of cold and warm water/air into the ear canal while supine) Loss of utricular afferent neuron signaling to the brain ↓ or absent Ocular Vestibular- Evoked Myogenic Potentials (VEMPs) and Normal Cervical VEMPs ↓ unilateral vestibular input to the brain leads to acute phase symptoms (over time, brain can compensate which allows for some symptom improvement) Loss of posterior SCC and saccular afferent neuron signaling to the brain ↓ or absent Cervical VEMPs, but Ocular VEMPs are normal ↓ or absent input to the ipsilateral vestibular nuclei elicits a vestibular nucleus response similar to contralateral SCC excitation Acute-Phase Spontaneous Nystagmus Fast phase beats away from the affected side (3- 10 days) And Loss of ocular fixation on Head Impulse Test ↓ or absent saccular input to the lateral vestibular nuclei (e.g., lateral vestibulospinal tract) results in the loss of lower limb postural adjustability Postural Instability (e.g., abnormal Romberg/sharpened Romberg, Fukuda step test) Bilateral mismatch of vestibular information to the brain Peripheral Vertigo (lasts several hours to days; rapid onset, severe, constant) Nausea and Vomiting Only the vestibular part of the vestibulo- cochlear nerve is affected, not the cochlear nerve No Hearing Loss or Tinnitus Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 19, 2021 on www.thecalgaryguide.com

BPPV

Benign Paroxysmal Positional Vertigo (BPPV): Pathogenesis and Clinical Findings Authors: Ryan Chan, Jonathan Wong, Mehul Gupta, Yan Yu* Reviewers: Davis Maclean, Saud Sunba, Euna Hwang* * MD at time of publication Up-beating, torsional geotropic (towards the ground) fast-phase nystagmus (towards affected side) Down-beating +/-torsional fast-phase nystagmus (towards opposite side) Idiopathic Older Age Head trauma Recent Ear Surgery Underlying Vestibular Disorders/Infections: Meniere’s Disease, Vestibular Neuritis, Labyrinthitis Risk Factors of Labyrinth Ischemia: Hypertension, Hyperlipidemia, Migraines Dislodged otoliths/otoconia from the macula of the utricle Posterior Canal BPPV (~95-99%) Superior Canal BPPV (~1%) Horizontal Canal BPPV (~5-20%) Ocular muscles are stimulated to generate a downward, torsional slow-phase movement Ocular muscles are stimulated to generate an upward, torsional slow-phase movement Cupulolithiasis Theory: Otolith adheres to cupula of the semicircular canal (SCC) Otolith displaces the cupula during head position changes resulting in prolonged sense of head rotation along the semicircular canal axis OR Canalithiasis Theory: Free-floating otolith in the semicircular canal (SCC) Otolith induces inertial drag of the endolymph fluid during motion, displacing the cupula, resulting in prolonged sense of head rotation Dix-Hallpike Maneuver: Sitting with head rotated laterally (45°), moving quickly to supine with head extended 30° off table. Observe for any nystagmus. Direction of nystagmus indicates which of the three semicircular canals is affected. Ocular muscles are stimulated to generate a horizontal slow-phase movement away from affected side Horizontal Nystagmus: Fast phase beats toward the affected side Supine Head Roll Test: lying supine, roll head laterally to each side to move otoliths along horizontal SCC axis BPPV: Episodic, positional bouts of vertigo and nystagmus not due to an underlying neurological or insidious reason If the otolith is free-floating in the SCC, movement of the affected ear towards the table generates a net stimulatory endolymph flow in the affected horizontal SCC The stimulatory signal is carried to brainstem nuclei, generating a reflexive slow movement of the eyes away from the affected ear, and quick horizontal movements back towards the affected ear Geotrophic Horizontal Nystagmus: fast-phase nystagmus beats horizontally towards the table If the otolith is adherent to the SCC cupula, movement of the affected ear towards the table generates a net inhibitory deflection of the horizontal SCC cupula The inhibitory signal is carried to brainstem nuclei, generating a reflexive slow movement of the eyes towards the affected ear, and quick horizontal movements away from the affected ear Apogeotropic Horizontal Nystagmus: fast-phase nystagmus beats horizontally towards the ceiling Otoconia & otoliths only affect the semicircular canal (SCC), not the cochlea No tinnitus or hearing loss Otoconia tend to settle quite quickly (<1 min) when body is still, resolving the mismatch of body movement & semicircular canal (SCC) excitation Vertigo and nystagmus is transient (lasting ~1min or less) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 9, 2022 on www.thecalgaryguide.com

Migraines and auras pathogenesis and clinical findings

Migraines and Auras: Pathogenesis and clinical findings Genetic mutations at certain loci (e.g., Familial hemiplegic migraine mutation in gene encoding P/Q-type Ca2+ channels) Personal triggers (e.g., lack of food, emotional stress) “Cortical Spreading Depolarization” followed by “Cortical Spreading Depression” across one cortical hemisphere Cortical spreading depression creates “auras” via unknown mechanism(s) Expanding scotoma (area of visual blurriness) Spreading paraesthesias (numbness that travels across body) Dysphasic language (trouble finding words) Brainstem symptoms (e.g., vertigo, tinnitus) Motor symptoms (e.g., hemiplegia) Triggering of a depolarization wave in a unilateral region of the cortex with associated ↑ blood flow to that region Neurons and glia release K+ into extracellular space that spreads depolarization wave to nearby cortical areas Ion gradient imbalances cause Prolonged vasoconstriction neurons in original cortical area to and ↓ blood flow swell and become inhibited Activation of the hypothalamus (responsible for maintaining homeostasis) Prodromal symptoms (↑ thirst, hunger, yawning, ↓ cognitive function) Author: Yan Yu Braxton Phillips Reviewers: Shahab Marzoughi Owen Stechishin Dustin Anderson Scott Jarvis* Sina Marzoughi* * MD at time of publication Release of hypothalamic neurotransmitters (e.g., orexins, neuropeptide Y) at the trigeminalcervical complex (TCC) of the brainstem and cervical spinal cord Depolarizing wave passes over pseudounipolar neurons (neurons with two axons) of the trigeminal ganglion which synapse in brainstem & dura matter These neurotransmitters reduce the activation threshold of spinal trigeminal nucleus neurons in the TCC Neuropeptides (e.g., calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide) are released at the TTC, triggering local inflammation (termed neurogenic inflammation) Ongoing neurogenic inflammation activates secondary nociceptive neurons in the TTC Central sensitization (↓ response threshold of secondary nociceptive neurons in the TTC) Brain perceives referred pain from the face as the TTC also receives convergent nociceptive input from the face Facial allodynia (pain with normally non-painful stimuli) Serotonin & histamine are released on dural blood vessels triggering neurogenic inflammation in the dura matter Ongoing neurogenic inflammation activates primary nociceptive neurons in the dura matter Peripheral sensitization (↓ response threshold of primary nociceptive neurons around the dural blood vessels_ Unknown mechanisms no longer believed to be related to dural blood vessel dilation Unilateral throbbing headache Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Nov 22, 2012, updated Jul 1, 2024 on www.thecalgaryguide.com

Polycythemia Vera Complications

Polycythemia Vera (PV): Complications High numbers of cells & platelets ↑ blood viscosity Polycythemia Vera Hematological disorder in which JAK2 mutations in hematopoietic cells result in increased RBC production. See corresponding Calgary Guide slide “Polycythemia Vera: Pathogenesis” ↑ Blood cell volume Presence of increased numbers of platelets creates a hypercoagulable and prothrombotic state ↑ Risk of venous & arterial thrombosis ↑ Systemic vascular resistance Impaired/“sluggish” blood flow ↓ Perfusion to small vessels and ↓ oxygen delivery to throughout body Arterial clots in arms and legs or in vessels leading to brain prevent oxygen delivery to cells Systemic hypertension ↑ Turnover of hematopoietic cells (RBCs, WBCs, platelets) Fatigue Transient visual disturbances Neurological symptoms (e.g. headache, dizziness, tinnitus, concentration problems) Breakdown of nucleic acids during cell turnover ↑ uric acid levels in blood Lysing cells release lactate dehydrogenase (LDH) into bloodstream ↑ Spleen activity to filter and dispose of old blood cells Splenomegaly Authors: Caitlin Bittman Noriyah Al Awadhi Yan Yu Peter Duggan* Reviewers: Maharshi Gandhi Kevin Zhan Michelle J. Chen Paul Ratti Merna Adly Crystal Liu Kareem Jamani* Man-Chiu Poon* Lynn Savoie* * MD at time of publication Extramedullary hematopoiesis Pancytopenia Clots in the portal vein, splenic vein, & mesenteric vein are unusual & highly suggestive of PV Clots in cardiac arteries prevent O2 delivery to cardiac tissue Myocardial infarction Venous blood moves more slowly and is less pressurized compared to arterial blood. Combined with hypercoagulable state, clots are likely to form in deep veins (usually of the legs) Deep vein thrombosis Clot breaks off and travels through the inferior vena cava & right heart into the pulmonary arteries Pulmonary embolism Stimulation fibroblasts in the bone marrow Uric acid accumulates & precipitates in blood Hyperuricemia ↑ Serum LDH Limb ischemia Ischemic stroke & transient ischemic attacks Erythromelalgias (burning pain in the extremities and erythema due to poor perfusion and transient microvascular occlusion) Compensatory vasodilation in the capillaries of the skin Plethora/rusted or “ruddy” complexion, particularly noticeable on the face, palms, nailbeds, & mucous membranes Gout Uric acid stones Advanced Disease Progression Abnormal blood cells produced in PV release various growth factors and cytokines Production of excess collagen and other fibrous materials Hematopoietic cells in bone marrow replaced with fibrous tissue over time Bone marrow increasingly unable to produce healthy blood cells Myelofibrosis (rare type of chronic blood cancer; considered late-stage progression of PV characterized by bone marrow fibrosis) Bone marrow failure Chronic bone marrow hyperactivity leads to exhaustion and/or damage of hematopoietic cells Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Aug 7, 2012, updated Feb 22, 2025 on www.thecalgaryguide.com