BMS Exam 3.docx

BMS Exam 3- Dra. Gil Lecture 1: Nose, Pharynx, Larynx Respiratory System Conduction Portion: upper respiratory system- nose and pharynx Filter, warm, and moisten air; conduct it to the lungs Respiratory Portion: larynx, bronchi, and lungs (where gas exchange occurs) Nose External Portion (carti...

BMS Exam 3- Dra. Gil Lecture 1: Nose, Pharynx, Larynx Respiratory System Conduction Portion: upper respiratory system- nose and pharynx Filter, warm, and moisten air; conduct it to the lungs Respiratory Portion: larynx, bronchi, and lungs (where gas exchange occurs) Nose External Portion (cartilage framework) Septal cartilage, Lateral nasal cartilages, Alar cartilages (part of the walls of the nostrils) Covered with muscles and skin Internal Portion (connects w the pharynx through two internal nares) Nasal cavity, divided by the nasal septum Nasal concha: superior, middle, and inferior Lined with mucous membrane Functions Warms, moistens, and filters air (hair in nostrils help filter large particles) Detect olfactory stimuli Contribute to voice resonance Olfactory Epithelium Olfactory receptors on the membrane lining the superior nasal conchae and the nasal septum Pseudostratified columnar epithelium secretes mucous to trap particles Blood capillaries warm incoming air Nasal Foreign Bodies Young patients, mentally ill Unilateral, foul-smelling, or bloody/purulent rhinorrhea Topical Phenylephrine for removal with nasal speculum and Hartmann nasal forceps Nose Clinical Correlation Epistaxis Nose bleeding, ranging from a trickle to a strong flow Most bleeds are anterior and stop w direct pressure and vasoconstrictors Posterior bleeds back into the throat, and is treated with gauze compression or balloon posterior pressure Screen for bleeding disorders, and ask about aspirin and ibuprofen use Rhinitis Inflammation of the nasal mucous membrane Symptoms: nasal congestion, rhinorrhea (runny nose), and other associated symptoms Causes: usually viral (common cold), or irritants Treatment: humidification, antihistamines, decongestants Bacterial superinfection- antibiotic treatment Types of Rhinitis Acute: cough, low grade fever, congestion, rhinorrhea, and sneezing Chronic: similar to acute, but prolonged or severe Thick, foul-smelling, mucopurulent drainage & mucosal crusting and/or bleeding Atrophic (atrophy): crust formation, anosmia, epistaxis that may be recurrent or severe Anosmia Complete loss of smell (hyposmia is a partial loss of smell, which is normal with aging) Causes: URI, sinusitis, and head trauma (cranial imaging needed if cause is not obvious) Other causes: olfactory neuroepithelium is destroyed Pharynx Funnel shape tube, from internal nares to the cricoid cartilage (larynx) Functions: passageway for air and food, voice resonance, and house the tonsils Uvula hangs in the midline at the far end of the soft palate Tonsils and adenoids are patches of lymphoid tissue surrounding the posterior pharynx Pharynx Divisions Nasopharynx: entrance of air Oropharynx: pass food, drinks, and air (two paths, one from mouth and one from nose) Laryngopharynx: opens into the esophagus and larynx Pharynx Clinical Correlations Pharyngitis (sore throat) Pain in posterior pharynx (w & w/o swallowing) Most common cause: tonsillopharyngitis (rarely abscess or Epiglottitis) Tonsillopharyngitis Viral Infection is the main cause (respiratory virus: rhinovirus, adenovirus, influenza, RSV) Few caused by bacterial infection (GABHS most common bacteria) Signs: tonsillar exudate, tender lymphadenopathy, fever, absence of cough Pharyngeal Abscess Abscess in the pharyngeal area: Peritonsillar, Parapharyngeal, Retropharyngeal (children) Uncommon, but significant throat pain Usually, cause is GABHS Treatment: BS-Antibiotic, saltwater gargle, topical anesthetics Epiglottitis Fever, respiratory distress, abrupt onset of severe throat pain and dysphagia Usually, no preceding URI symptoms Drooling, muffled voice (hot potato voice) Primary in children (Hemophilus Influenzae B) Seve sore throat in a patient with a normal appearing pharynx should raise suspicions of this Sialadenitis Bacterial infection of salivary glands, usually due to an obstructing stone or gland hyposecretion More common in the parotid gland, in patients in their 50s & 60s, xerostomia, and radiation therapy Most common agent: Staphylococcus Aureus S&S: fever, chills, unilateral pain, swelling, and tenderness. Erythema and edema of the overlying skin Pus can often be expressed from the duct Focal enlargement may indicate an abscess Diagnosis: CT, Ultrasound, MRI, Gram stain, culture Treatment: antibiotics, warm compresses Adenoids Rectangular mass of lymphatic tissue in the posterior nasopharynx (largest in 2-6 y/o) Enlargement may be secondary to viral or bacterial infection, allergy, irritants, and possible gastroesophageal reflux Severe hypertrophy can obstruct the Eustachian tubes (causing Otitis Media) Adenoiditis (hypertrophy or inflammation common in children) Symptoms: nasal obstruction, sleep disturbances, mouth breathing, middle ear effusions w hearing loss, hypo-nasal voice, halitosis, recurrent otitis media (middle ear inflammation) Diagnosis: flexible nasopharyngoscopy Treatment: frequent otitis media-adenoidectomy, treat allergy w cortio, infection w antibiotics Larynx Voice box, connects Laryngopharynx w Trachea Part of the lower respiratory system Cartilaginous walls Thyroid: Adams apple, anterior Cricoid: inferior Arytenoid: posterior Epiglottis: elastic cartilage that moves over the larynx during swallowing Glottis: true vocal cords and the space between them Voice production Vestibular folds (false vocal cords): one or two pairs of mucous membrane folds Vocal cords (true vocal cords): one pair of deep bands of elastic ligaments A persistent change in the voice (>3wks) require visualization of the cords (laryngoscopy) Larynx Clinical Correlation Laryngitis: inflammation of the larynx Usually result of virus or overuse (viral laryngitis is self-limiting) (bacterial is extremely rare) Other causes: allergic reaction, gastro reflux, bulimia, or inhalation of irritating substances Laryngoscopy required for symptoms persisting after 3 weeks Drugs can induce laryngeal edam (ACE Inhibitors) Diagnosis: clinical evaluation, sometimes direct or indirect laryngoscopy Treatment: symptomatic treatment (cough suppressants, voice rest, steam inhalation) Polyps, Nodules, and Granulomas Caused by acute trauma or chronic irritation (judicious surgical removal restores the voice) Hoarseness and a breathy voice Diagnosis: laryngoscopy, sometimes biopsy Polyps (unilateral) Result of injury to the lamina propria of the true vocal cords Occur at the mid third of the membranous cords Other causes: gastro reflux, hypothyroid, chronic laryngeal allergic reactions, chronic inhalation of irritants Larger and more protuberant than nodules Nodules (bilaterally) Occur at the junction of the anterior and middle third of the cords Due to chronic voice abuse Granulomas Occur in the posterior glottis against the vocal process Can be uni- or bilateral Usually from intubation trauma (aggerated by reflux disease) Carotid Auscultation Bruits: rushing sound heard over medium and large arteries, caused by vibrations of the blood vessels induced by turbulent flow Atherosclerotic plaque: more common at the proximal and distal ends of the CCA, where it bifurcates Indications: Amaurosis fugax (transient loss of vision), TIA, Hollenhorst plaque, Retinal Occlusion Process (bell-low frequency, heart and vascular sounds) (diaphragm-high frequency sounds, lungs) 1 inch above clavicle, ask to stop breathing mid-expiration, listen, and resume breathing Repeat 2-3 times along length of the carotid and the other side Palpation of the Carotid Pulse (grade 0-4, no pulse to bounding forceful pulse) Atherosclerotic plaque will reduce carotid blood flow, evident by diminished pulse palpation Lecture 2: Neurotransmitters Classification Functional: excitatory or inhibitory Effects: direct or indirect NRTM termination Degradation by enzymes Reuptake by astrocytes or the presynaptic cell Diffusion away from synapse Acetylcholine Excitatory, synthesized from Choline and Acetyl CoA CNS: through cerebral cortex, hippocampus, and brain stem PNS: neuromuscular junction with skeletal muscles and all preganglionic and parasympathetic postganglionic fibers Receptors: Nicotinic N1: adrenal medulla and autonomic ganglia Nicotinic N2: skeletal muscle Muscarinic M1-M5: widely distributed in the CNS M1 in the ANS, striatum, cortex, and hippocampus M2 in the ANS, heart, intestinal smooth muscle, hindbrain, and cerebellum Regulate movement, cortical excitability, arousal and sleep, and cognition and reward Exposure to organophosphate insecticides create a prolonged effect that causes titanic muscle spasms Inhibited by botulism toxin ACh decreased in certain areas in the brain with Alzheimer’s Nicotinic ACh receptors destroyed in Myasthenia Gravis ACh Clinical Correlation Huntington’s Disease Result from degeneration of ACh and GABA containing neurons Patients have chorea (contraction of proximal muscles), and dementia Myasthenia Gravis Autoimmune syndrome: presence of antibodies against Nicotinic ACh receptors, resulting in paresis EOM & Eyelid Muscles (diplopia & ptosis), bulbar muscles (nasal speech and jaw fatigue) Weaker limbs proximally and stronger limbs distally Diagnose with IV Edrophonium (a reversible AChE inhibitor) Use of muscles results in fatigue Lambert-Eaton Myasthenic Syndrome Presynaptic deficit of ACh release, causing weakness on the limb muscles 50% associated with neoplasms (lung, breast, prostate) Muscle strength improves with use Dopamine Catecholamine (produced by the adrenal gland) Can be excitatory or inhibitory dependent on the receptor type Secreted at CNS: Substantia Nigra of Midbrain and Hypothalamus PNS: Some Sympathetic Ganglia Receptors D1 through D5 D3 & 4 play a role in thought control D2 controls the extrapyramidal system (voluntary movements) Feel good neurotransmitter (L-dopa and amphetamines enhance) Increased production in schizophrenics Mainly controls movements and pleasure Dopamine Clinical Correlation Parkinson’s Disease Loss of dopaminergic neurons in the Substantia Nigra Tremors, rigidity, and akinesia (loss of ability to make voluntary muscle movements) Norepinephrine Catecholamine Excitatory or Inhibitory dependent on receptor type Location CNS: brain stem (locus coeruleus), limbic system, some areas in cerebral cortex PNS: main NRTM of ganglion neurons in the sympathetic nervous system Receptors Alpha 1: postsynaptic in the sympathetic system Alpha 2: presynaptic in the sympathetic system and postsynaptic in the brain Beta 1: heart Beta 2: other sympathetically innervated structures Maintenance of mood Amphetamines enhance release Reduced norepinephrine is related to depression, and increased is related to Mania Serotonin (5-Hydroxytryptamine, 5-HT) Mainly Inhibitory (indirect via second messengers, direct at 5-HT receptors) Location: Brain stem (specifically midbrain), Hypothalamus, Limbic System, cerebellum, penial gland, spinal cord Receptors (Serotoninergic receptors w at least 15 subtypes) 5-HT1 (4 subtypes) 5-HT2 5-HT3 Role in sleep, appetite, nausea, migraine headaches, regulation of mood, body temperature, and pain Severe depression and insomnia related to low levels of 5-HT, and Mania is associate with high levels OCD is related to dysfunction of 5-HT Tricyclic Antidepressants and Fluoxetine increase 5-HT availability Selective serotonin receptor agonists can abort migraines via vasoconstrictive and anti-inflammatory effect Lecture 3: Paranasal Sinuses and Ear Paranasal Sinuses Lined w mucous membranes, continuous with the lining of the nasal cavity Produce mucous, lighten the skull, and serve as a resonating chamber for sound Cavities are in the Frontal, Sphenoid, Ethmoid, and Maxillary bones Frontal and Sphenoid sinuses are more evident in a SAGITAL SECTION Ethmoidal and Maxillary sinuses are more evident in the FRONTAL SECTION Orbit and Paranasal Sinus Relation Close relation between Paranasal Sinus and Orbit (60-80% of the orbit is made by the sinus walls) Ethmoid cells represent the thinnest wall (Lamina Papyracea-sounds like paper) Extension or compression of the soft tissue leads to Exophthalmos (proptosis) Mechanical restriction of Superior Oblique leads to diplopia Maxillary sinus disease is rare but can occur after an orbit floor fracture Sphenoid sinus and ethmoid cells are attached to the Orbital Apex (disease causes exophthalmos or different CN alterations) Sinusitis Inflammation of paranasal sinuses (bc Viral, Bacterial, or Fungal Infections or Allergic reactions) Enough swelling can cause blocked drainage leading to sinus headaches Severely deviated nasal septum or nasal polyps may also cause chronic sinusitis Acute: resolved in less than 30 days Subacute: resolved in 30-90 days Recurrent: 4 or more discrete acute episodes per years (each resolved in less than 30 days) Chronic: last more than 90 days Symptoms include Nasal Obstruction (congestion), Purulent Rhinorrhea, Facial pain or pressure, HAs, fever Etiology Viral: Rhinovirus Secondary bacterial infection: Strep Dental Abscess of maxillary tooth spreads to overlying sinus Hospital-Acquired acute infection: Staph Immunocompromised patients may have Acute invasive Fungal Sinusitis: Aspergillus Diagnosis: x-ray (Caldwell and waters view), CT scan (Chronic) Treatment: Phenylephrine, Pseudoephedrine (vasoconstrictors), Oral AB, unresponsive (surgery) Immunocompromised Patients: aggressive and even fatal fungal or bacterial (DM, neutropenia, HIV) Mucormycosis Mycosis Black, devitalized tissue in nasal cavity Neurologic signs: secondary to retrograde thromboarteritis (inflammation of artery w/ thrombosis formation) Treatment: control of underlying condition, Amphotericin B Aspergillosis and Candidiasis May infect Paranasal Sinuses (secondary to therapy w Cytotoxic drugs) (immunosuppressive disease) Treatment: aggressive paranasal sinus SX, IV Amphotericin B Cavernous Sinus Thrombosis Very rare complication of common facial infections Nasal Furuncles 50%, Sphenoidal or Ethmoidal Sinusitis 30%, Dental Infections 10% Most common pathogen is Staph Aureus 70% CN 3, 4, and 6 and Ophthalmic and Maxillary branches of CN 5 are adjacent to Cavernous Sinus are commonly affected Signs/Symptoms Periorbital Edema may be the earliest physical finding Chemosis results from occlusion of Ophthalmic Veins Ophthalmoplegia (lateral gaze palsy): isolated CN 6 is usually seen first (les freely within the sinus composed to the others that lie within the walls Ptosis, Mydriasis, Anisocoria, and EOM weakness from CN 3 dysfunction Exophthalmos’s from increased retrobulbar pressure Increased IOP Decreased VA or vision loss Papilledema on the ONH Hypoesthesia or Hyperesthesia Diagnosis: MRI is best, but CT is helpful Complications: Meningoencephalitis, brain abscess, stroke (mortality in 30% of patients, and 50% in those w underlying sphenoid sinusitis) Treatment: AB IV-Vancomycin, sometimes corticosteroids (CN dysfunction) External Ear Three Regions Auricle: elastic cartilage to collect sound waves External Auditory Canal: located in temporal bone Tympanic Membrane: sound waves cause it to vibrate Contains hairs, and cerominus glands (sebaceous glands) Prevents dust and foreign objects from entering the ear, and directs sound waves to the TM Middle Ear Air filled cavity in the Temporal bone Has three small bones that transmit and amplify vibrations from the TM to the orbital window Malleus Incus Stapes Connected to the Nasopharynx by the Eustachian Tube Equalize Atmospheric Pressure on BOTH sides of the TM Internal Ear Bony Labyrinth: Semicircular canals, the vestibule (receptors of equilibrium), cochlea (hearing), contains perilymph (similar to the CEF) that surround the membranous labyrinth Membranous Labyrinth: contains endolymph The Vestibule contains two sacks, Utricle & Saccule Three Bony semicircular canals contain ducts that communicate with the utricle Vestibular branch of vestibulocochlear nerve receives info from the vestibule and semicircular canals Inner Ear The cochlea contains 3 interior channels and Spiral Organ/Organ of Corti (in basilar membrane) Organ of Corti Contains hair cells, receptors for hearing Apical end of hair cells extend to the endolymph of the cochlear duct and is covered by Gelatinous Tectorial Membrane Basal end of hair cells synapse w sensory neurons from the Cochlear band of the CN8 Equilibrium Static: maintain body position relative to gravity Dynamic: response to sudden movement (rotation, acceleration, deceleration) Organs of Equilibrium: Saccule, Utricle, and Semicircular Ducts 3 semicircular ducts function in dynamic eq Each Ampulla (distal end of the semicircular duct) has an elevation or Crista that contains a group of hair cells and supporting cells covered by Gelatinous Cupula Movement causes the endolymph to move through the ducts and bend the hair Macula consists of hair cells that act as Sensory Receptors Receptors for static equilibrium also contribute to dynamic equilibrium Otolithic Membrane cover the hair cells that are covered by Otoliths (calcium carbonate crystals that amplify the pull of gravity during movements) Clinical Applications for the Ear Perforated Eardrum: usually heals within a month Impacted Cerumen: earwax Foreign Bodies External Otitis Normal TM Itching and Pain-History of swimming or recurrent water exposure Canal red and swollen with Purulent debris Barotrauma (baro-pressure) Often Hemorrhage on or behind the TM Significant pain-History of rapid change in air pressure Otitis Media Bulging, red TM Significant pain-often URI symptoms More common w children Acoustic Neuroma (Vestibular Schwannoma) Tumor of CN8, as it expands it projects into the cerebellopontine angle (compressing CN7, CN8, and even CN9 & 12) Symptoms: unilateral hearing loss Treatment: surgical removal or Stereotactic radiation therapy Benign Paroxysmal Positional Vertigo (most common cause of vertigo) Displacement of otoconial crystals (displacement stimulates hair cells, commonly in Posterior SC) Can be caused by many things including concussion, otitis media, ear sx, infection, or bed rest S/S: triggered when the patients head moves, peak in the morning NO HEARING LOSS/TINNITUS Nausea and vomiting may occur Treatment: repositioning maneuvers (drugs may make condition worse) Meniere Disease (vertigo) HEARING LOSS & TINNITUS Treated symptomatically (nausea) w diuretics and low-salt diet are first line Pressure and volume changes of the Labyrinth Endolymph affect inner ear function Family history is a risk factor Ototoxic Drugs Aminoglycosides (-cin) (Gentamycin, Streptomycin, Neomycin…) & Glycopeptides (vancomycin) Chemo Drugs: platinum containing drugs Diuretics: furosemide Antimalarial Salicylates Lecture 4: Organic Diseases of the CNS Meninges: coverage of the brain, transparent Edema: swelling of the brain, meninges get tight and can break Vasogenic: BBB dysfunction (interstitial: increased CSF in the ventricles) Mainly by tumors Cytotoxic: osmotic imbalance Ischemia, trauma Both can occur together Edema Etiology Space Occupying lesions: Malignancies, Hydrocephaly (interstitial swelling) Post traumatic Metabolic disorders: Hyperglycemia Herniation Anatomical Factors: rigidness of cranial vault & Dural reflections Subfalcine (affect behavior and memory) Herniation of Cingulate Gyrus under the Falx Cerebri (compress Corpus Callosum and Ventricles) Anterior Gyrus regulates motivation, attention, and behavior (pt become aggressive) Posterior Gyrus regulates learning and memory (lose short term memory) Tonsillar Displacement of Cerebellar Tonsils through the Foramen magnum resulting in compression of the Brain Stem Increase of CSF, causes cerebellum to be pushed down Transtentorial Temporal lobe compressed against the free margin Tentorium Cerebri (invagination of the meningeal layer of the dura mater that separates the occipital and temporal lobes of the cerebral hemispheres from the cerebellum and brainstem) w compression of CN3 Dilated Pupil, impaired ocular movement of ipsilateral side Compression of Posterior Cerebral Artery resulting in ischemic injury to visual cortex Diagnostic Tests CT Scan: first one bc fastest MRI: look for ischemia and tumors Surgical: Drainage and Excision Diuretics: Mannitol (first line TX for edema, restores ICP and removes swelling) Hydrocephalus Accumulation of CSF Communicating (Non-obstructive, extra-ventricular) Obstruction is outside of the ventricles Expanding tissue swelling ependymal cells start overproducing CSF Non-Communicating (Obstructive, intra-ventricular) Obstruction is at the ventricular level CSF not passing through Diagnostic Test: CT Scan, MRI Treatment: surgical drainage Cerebrovascular Disorders Generalized reduction of blood flow that leads into hypoxic ischemic injury in water shed area (Dural supply from two arteries) which are junctions between: Anterior and Middle Cerebral Arteries & Superior and Inferior Cerebellar Arteries Review of arteries Anterior Cerebral Artery (ACA): medial portions of the frontal and parietal lobes and corpus callosum Middle Cerebral Artery (MCA): portions of the frontal, parietal, and temporal lobe Branches from ACA and MC (lenticulostriate arteries): basal ganglia and anterior limb of the internal capsule Vertebral and Basilar Arteries: brain stem, cerebellum, posterior cerebral cortex, and medial temporal lobe Posterior Cerebral Arteries: bifurcate from the basilar artery, supply the medial temporal (including the hippocampus) and occipital lobes, thalamus, and mammillary and geniculate bodies Vascular Disorders (lack of entrance of blood) Normal Circumstances: brain receives 15% of cardiac output & consumes 20% of the total oxygen consumption Parenchymal Lesion: reduction of blood supply Infarcts (secondary to vascular disorders) Hemorrhages (secondary to vascular disorders) Infarction 80% result from local vascular occlusion (hemorrhages w/in the parenchyma or subarachnoid space) More common in males after 70 years old More common in areas supplied by the MCA Predisposing factors: HTN, DM, Atherosclerosis, smoking Stroke and TIA Stroke: sudden, focal interruption of cerebral blood flow, causes deficit (ischemic 80%, hemorrhagic 20%) TIA: stroke symptoms lasting less than 1 hour, DO NOT cause damage (pt will not have ischemia) 35% TIA recur in a stroke 3rd most common cause of death and most common cause of neurologic disability (developed countries) Risk Factors: prior stroke, males, HTN, hypercholesterolemia, DM, drugs S/S: initial symptoms occur suddenly Numbness, Paresthesia (tingling or numb feeling), weakness/paralysis of CONTRALATERAL limbs and face, Aphasia, visual disturbances in one or both eyes Neuro Deficits reflect the area of the brain involved Anterior Circulation: Unilateral symptoms Posterior Circulation: uni-or bilateral (more likely to affect consciousness, especially w Basilar Arter involvement) Most are unilateral with contralateral effects Other manifestations that suggest stroke Sudden severe headache: subarachnoid hemorrhage Impaired consciousness/coma w headaches, N&V: increased ICP 48-72 hours after large ischemic stroke and earlier w hemorrhagic ones: fatal brain herniation Complications: sleep disorders, confusion, incontinence (no urine control), pneumonia, swallowing dysfunction Immobility leads to thromboembolic disease, UTIs, pressure ulcers, contractures of upper and lower limbs Alters daily function Stroke Evaluation-Aim to establish: Whether a stoke occurred, the type, and determine if immediate TX is required Suspect in: sudden neuro deficits, sudden/severe headache, coma, impaired consciousness Stroke Diagnosis CT is sensitive for intracranial blood (may be normal or show subtle changes during first few hours after symptoms of Anterior Circulation Ischemic Stroke) CT is first option for hemorrhagic stroke (if no bleeding do MRI) Always rule out Hypoglycemia (only thing that mirrors symptoms) Treatment for stroke (stabilize before complete evaluation) May need airway support (GCS <8) Monitor ICP Prevent and treat compilations Prevention and Treatment of Stroke Complications Elastic or air-filled stockings to avoid thrombosis Frequent repositioning to avoid pressure ulcers Passive exercise of limbs (compression socks) Anticoagulants Early walking, respiratory exercises Diagnostic Test CT Scan- plain w/ contrast strain MRI Treatment Surgical drainage Thrombolytic agents & Anticoagulants PT Hemorrhages Parenchymal (non-traumatic) Most common in 50-60 years of age HTN is the leading cause Congenital Disorders (mainly aneurysms) Trauma (without fracture that leads to edema) Aneurysms Saccular dilation (congenital defect in the media arteries at points of bifurcation) affecting Circle of Willis 80% arise at bifurcation of the internal carotid artery branches Affect 1% of people (more common in women before the 5th decade) Critical size 4-6mm Fixed surgically w clips, must be completed in 6 min to prevent irreversible brain damage Arteriovenous Malformation (AVM) Mostly due to Congenital Vascular Abnormalities in the brain Diagnostic Tests: CT Scan (w/ contrast first) & MRI Treatment: surgical drainage & pharm anti-HTN Trauma 70% of head trauma survivors are permanently disabled Epidural Hematoma: ruptured Meningeal Artery (above dura) Subdural Hematoma: disruption of bridging veins (below dura) Subarachnoid Hemorrhage: surrounding the parenchyma of the brain, commonly secondary to trauma Diagnostic Tests: CT w/ contrast, MRI Treatment: surgical drainage Traumatic Parenchymal Injuries: Concussion, Contusion, Coup (area of impact), Countercoup (damage in opposite side of impact) (common in shaken baby syndrome) Lecture 5: Infectious Diseases of the Brain Meningitis (inflammation of the Meninges, specifically Leptomeninges, the most internal) Two internal layers: Arachnoid and Pia Acute Purulent: mainly bacterial in nature (pus btw meninges, yellow) Acute Lymphocytic: mainly viral in nature (elevated WBC) Chronic Meningitis: association of low virulent bacterial and fungi Encephalitis: infection of brain parenchyma Acute Pyogenic (pus in the subarachnoid space) Aseptic (usually viral, no pus) Chronic (low grade bacteria, longer time) Etiology of Meningitis Community-Acquired Acute Bacterial Meningitis: Streptococcus Pneumoniae 50-60%, Neisseria Meningitides 14-37% Other frequent causes: Haemophiles Influenzae in pt w low immune status (3-4%), Listeria Monocytogenes (4-11%) Patients w prior neuro sx: Staph Aureus & Steph Epidermis Rare Etiologies Leptospirosis: history of exposure to rodent, dog, livestock, & associated Jaundice and renal dysfunction Parasites (through nose): amebic disease secondary to Naegleria Foweri and Acanthamoeba species in freshwater lake Acute: characterized by Cellular Pleocytosis (increased cell count esp WBC) in CSF Manifestations Headache Fever Meningismus (painful stiff neck) (Positive Kerning Sign & Brudzinski’s Sign) Severe neck stiffness causes a patients hips and knees to flex when the neck is flexed Peripheral nerves are inflamed Seizures, focal neruo deficits Disturbances of consciousness Signs and Symptoms Headache: severe frontal w photophobia and vomiting Fever: bacterial meningitis temp usually exceeds 99.6F (low grade often w Viral & absent in fungal) Stiff Neck Mental Status Change Bacterial-44% (most common) Viral-3% Seizures occur in 20-25% Focal findings as cranial nerve- 25-30% Diagnostic Differences between Etiologies Bacterial has increased PMNs while Viral and Fungal have an increase in Lymphocytes Viral can have all normal and only an increase in lymphocytes (normal glucose always) Bacterial and fungal appear very similar (difference is PMNs vs Lymphocytes) Acute Viral Meningitis Most common etiologies are Coxsackie Virus and Echoviruses DDX Encephalitis (inflammation of parenchyma): distinguished by absence of meningeal symptoms but presence of diffuse neuro deficits (commonly caused by HSV), Focal Brain Lesions can be detected by a CT scan Lecture 6: Brain Images CT Scan (computed tomography, lots of X-Rays) Dense tissue-more x-rays absorbed Bone: x-rays absorbed-white (dense) Air: x-rays not absorbed-black (less dense) Spiral CT: single source w multiple detectors Neurological Indications for Cranial CT Most indicated in ER evaluation of pts w acute had trauma and/or neurological dysfunction Looks for suspected intracranial or subarachnoid hemorrhage Useful for Vascular (ischemic stroke greater than 2 days old or acute hemorrhagic stroke) Trauma Hydrocephalus Tumor (primary CNS and metastatic) (contrast) Infection and Abscess (contrast) Contraindications for CT Pregnancy (potential harm exposing radiation to fetus) Use of intravenous contrast agents (Anaphylaxis, renal dysfunction, pts that take metformin should stop two days before) MRI (Magnetic Resonance Imaging) Generates extremely strong Magnetic Field and pulse radio frequency Align hydrogen nuclei in tissues and body water (subsequent loss of alignment with time produces the MRI signal) T1: water is dark-better for anatomy (soft tissue structures) T2: water is bright-better for pathology (inflammation and edema) Neurological Indication for Cranial MRI Vascular: Ischemic and Hemorrhagic Stroke, AVM, Aneurysm, Venous Thrombosis Tumor: Primary CNS and Metastatic Infection: Abscess, Cerebritis, Encephalitis, Meningitis Inflammatory/Demyelinating Lesions: MS, Sarcoidosis Trauma: epidural hematoma, subdural hematoma, contusion Hydrocephalus Congenital Malformations Limitations of MRI Subject to motion artifact Inferior to CT in detecting Acute Hemorrhage and Bony Injury Required prolonged acquisition for many images (Parkinson’s do not do well because of tremors) Contraindications to MRI Implanted devices and other metallic devices (pacemakers, aneurysm clips, cochlear implants, heart valves) Intraocular Foreign Body Unstable patients because you can’t take a crash cart into the room Pregnancy (unknown fetal effects) Severe agitation or claustrophobia MRA (Magnetic Resonance Angiography) Vessels are bright Useful for AVMs & Aneurysms (can be done w or w/o contrast) Lecture 7: Neurologic Disorders Approach to Neurologic Patients History/observation: symmetry, demeanor, and gait Mental Status: time, person, space Speech: express themselves and/or understand you Cranial Nerves Motor System: movement of limbs, face, and eyes Reflexes: stimulate terminal nerve in elbow to elicit Sensory system: cotton applicator to test sensation Common Neurologic Problems Headaches (constant and don’t disappear w meds) Speech problems, Confusion, Tremors, Unsteadiness, Numbness, Visual Symptoms, Weakness Disorder of consciousness (most important) Disorders of Consciousness Confused: disoriented, sleepy, or inattentive Delirium: depressed consciousness and elevated sympathetic tone (agitation, increase HR, BP, hallucinations) Obtunded: require repeated stimuli to maintain attention Stuporous: provide minimal repones to frequent or constant stimulation (sleepy state, react slowly) Coma: unresponsive Brain death: absence of brainstem reflex and apnea Diagnostic Approach Alteration of consciousness is a medical emergency Determine cause: trauma, seizures, previous complaints, history, medications used and/or abused Neurologic Evaluation Assessment of degree of disturbances (revised Glasgow Coma Scale (GCS)) Eye Opening, Motor Response, Verbal Response GCS <15: brain imaging and observation GCS < 9: indicative of coma (airway management) Periorbital Ecchymosis (racoon eyes) Severe head trauma, fractures at the base of the anterior cranial fossa Bleeding from ICA Postauricular Ecchymosis (battle signs) Fracture of temporal bone, mastoid cells are filled w more air and can break Bleeding near the mastoid process Management of Ecchymosis?? Immobilization of Cervical Spine Administer Thiamine, Naloxone, Glucose (hypoglycemic patients) Hyperventilation Mannitol IV for ischemia and swelling Imaging Studies CT: rapidly detect true hemorrhage and various gross structures CT w/ Angiography: Ischemic Stroke or SAH MRI: visualize pathology or brainstem, infarcts and diffuse injury in encephalitis, and laminar necrosis Lab Tests Serum: glucose, electrolytes, liver and renal function, coagulation tests, cardiac enzymes, drug screen Lumbar Puncture: spinal tap Acute Bacterial Meningitis, Acute Syphilitic Meningitis, Lyme Disease of CNS, brain Abscess or tumor, Guillain-Barre syndrome Electroencephalographs (EEG) Seizures: toxic or metabolic Multiple Sclerosis Disease of the White Matter in CNS Autoimmune w Perivascular Demyelination (genetic & environmental factors) First degree relatives- 10% increased risk Peak incidence in young adults between ages of 20-30 Myelin gets inflamed or damaged causing demyelination (plaques, visible in MRIs) Diagnosis: careful history, neuro exam, diagnostic MRI, confirmatory lumbar puncture Spinal Tap-Electrophoresis: normal-uniform bands, MS-thick bands throughout Usually starts w weakness: DDX Myasthenia Gravis Main Symptoms of MS Central: fatigue, cognitive impairment, depression, unstable mood Visual: nystagmus, optic neuritis, diplopia Speech: dysarthria (can’t speak correctly) Throat: dysphagia Musculoskeletal: weakness, spasms, ataxia Sensations: pain sensitive (naked nerves), paranesthesia, hypoesthesia (lose sensation) Bowel: incontinence, diarrhea, constipation Urinary: incontinence, frequency, retention Optic Neuritis in MS Sudden unilateral blindness, self-limited (2-3 weeks) Temporal pallor in Optics Disc Central scotoma due to acute retrobulbar neuritis Internuclear Ophthalmoplegia in MS Eyes Left: OD can’t adduct, OS abduction nystagmus Eyes Right: OD abduction nystagmus, OS lesser mild paresis Convergence: fully preserved adduction MS Clinical Courses Progressive Relapsing: steady decline bc superimposed attacks (acute episodes that increase, and increase demyelination) Secondary Progressive: initial relapsing-remitting that suddenly begins to have decline w/o periods of remission (relapsing episodes but it does not continuously increase) Primary Progressive: steady increase in disability without attacks (increase constantly until complete demyelination) Relapsing-Remitting: unpredictable attacks, may or may not leave deficits, followed by periods of remission MS Clinical Presentation Multiple attacks occur over a period of years (involves areas of white matter in the plaque formation process) R-R MS (relapsing-recurring MS) occurs 85% of cases, more common in younger women Often start with Prominent Sensory-Visual Symptoms Only subtype of MS that responds favorably to immunomodulatory therapies Chronic Progressive MS w/o remitting features seen in 10% of patient (later onset in males) Common Initial Symptoms in MS Paresthesia: one or more extremities experience weakness or clumsiness Visual Disturbances: partial loss of vision and pain in one eye due to Retrobulbar Optic Neuritis, Diplopia due to ocular palsy, and Scotomas Stiffness or fatigability of limb Minor gait disturbances Vertigo Ocular Manifestations in MS Unilateral or Asymmetric Optic Neuritis (causes loss of vision) Eye pain Abnormal Visual Fields Papilledema Afferent Pupillary Defect Bilateral Internuclear Ophthalmoplegia (lesion in the MLF connecting CN Nuclei III and VI) Horizontal gaze, adduction is decreased and nystagmus in abducting eye Convergence is spared (normal adduction) Treatment for MS Corticosteroids for Acute Exacerbations (Methylprednisolone IV) Immunomodulators to prevent Exacerbations (interferons) Supportive Care (physical and occupational therapy) Myasthenia Gravis (most common primary disorder of Neuromuscular transmission) Usually, an immunologic abnormality Genetic abnormalities with lack of receptors at neuromuscular junctions Incidence of 9 million per year, with a prevalence 200 per million population More common in women between 2nd-3rd decade of life, and males in 7th-8th decades Early onset associate with Thymoma (75-90%, Thymus Tumor) Presentation Complaint of specific muscle weakness rather than generalized fatigue Ocular disturbances are initial symptoms for 2/3 of patients (Ptosis and Diplopia) (almost all patients have both within TWO years) Oropharyngeal Muscle Weakness initial symptoms for 1/6 patients (Odynophagia, Dysphagia, Aphagia) Limb weakness in 10% of patients (weakness fluctuates during the day, better in the morning) Myasthenia Gravis Clinical Course Variable but progressive Symptoms are worse if accompanies by: Systemic Illness, Thyroid disease, Pregnancy, Menstrual cycle, drugs that impair neuromuscular transmission, increased body temp MG Diagnosis Weakness characteristically improves after IV admin of Edrophonium Chloride (AChE inhibitor, produces muscle contraction) Serum antibodies against human AChR are found in 70-90% of patients w acquired generalized myasthenia and 50-75% with ocular myasthenia but are not predictable for severity of disease Elevated concentrations of AChR-binding antibodies in a patient with compatible clinical features confirms the diagnosis MG Management Cholinesterase inhibitors cause improvement in some patients Pyridostigmine and Neostigmine (most common) Side effects: GI disturbances, increase bronchial and oral secretions (problems for patients with impaired swallowing or respiratory insufficiency) Prednisone: marked improvement or complete relief of symptoms occurs in >75% of patients Immunosuppressive Agents Mycophenolate Mofetil and Azathioprine reverse symptoms in more patients Cyclosporin Surgery: Thymectomy Tremors Causes your hand to shake rhythmically Head, trunk, and voice might also be involved Etiologies Physiologic Tremor Resting Tremor (Parkinsonian Tremor) Action Tremor Physiologic Tremor Stressful situation Hypermetabolic state (excess of thyroid hormones) Fever (tremors are trying to decrease temperature) Drugs Action Tremor Simple Kinetic Tremor Intention Tremor Task Specific Tremor Parkinson’s Disease Idiopathic, slowly progressive, degeneration CNS disorder Resting Tremor, Muscle Rigidity, Slow and decreased movement, postural instability 4th most common neurologic disorder in patients over 65 years old Prevalence: mean age at onset is about 57 years Parkinsonism refers to symptoms that are similar to those of Parkinson’s disease but caused by another condition such as dementia Parkinson’s Disease Pigmented neurons of the Substantia Nigra, Locus Coeruleus, and other brain stem dopaminergic cell groups are lost Genetic predisposition: 15-20% have family history AD for some genes and AR for others Levy Bodies: the pathological hallmark of Parkinson’s Result from accumulation of Synuclein (presynaptic protein) in the bodies of the Nigrostriatal System Patients w Parkinson’s may also have Alzheimer’s S/S Resting tremor of one hand often the first symptoms Characterized as being slow and coarse Maximal at rest, lessening during movement, and absent during sleep Amplitude increased by emotional tension or fatigue Treatment Levodopa & Carbidopa for the tremors Neuroblastive lesion surgery