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Neurological Disorders Structural Organization Brainstem & Cerebellum Cerebral hemispheres Spinal and Cranial Spinal Cord Nervous System Function Sensory Inputs afferent Brain: Central Processing Unit efferent Secretion Movement Sensory Tracts anterolateral dorsal Major Sensory Tracts Anterolateral (Spinothalamic) crosses immediately in the cord sensation is poorly localized itch, pain, temp Dorsal column ipsilateral until medulla, then crosses sensation is well localized touch, vibration, pressure, Major Motor Tracts Lateral Corticospinal crosses at medulla innervates distal muscles fine motor control Medial Tracts some tracts cross at medulla, some don’t innervates axial muscles balance, gross motor How Do Neurons Communicate? dendrite axon terminal axon synapse postsynaptic neuron Neurotransmitter Classes Acetylcholine Amines (DA, NE, E, 5HT, histamine) Amino acids (glutamate, GABA, glycine) Purines (adenosine) Gases (nitric oxide) Neuropeptides (Sub P, endorphins, AII, oxytocin, many others) Head Trauma / Bleeds Focal: localized Polar: acceleration-deceleration Diffuse: widespread disruption Determinants of Intracranial Pressure Three space occupying components Brain CSF Blood Compensation for Increased ICP CSF shunt to spinal cord Hyperventilation leading to vasoconstriction Causes of Increased ICP Brain infection Rupture of blood vessels Hydrocephalus F & E imbalances Head Injury – most common Types of Injury Primary injury Secondary injury Pathophysiology of Secondary Injury Ischemia Release of glutamate ATP deficiency Na+, Ca++ in cell “excitotoxin” cell damage vasospasm platelet plug Activation of phospholipases free radicals prostaglandins thromboxanes mitochondria dysfunction Compensation for Increased ICP Brain Swelling CSF shunted to spinal cord CSF in brain ventricles ICP Hyperventilation PaCO2 Cerebral vasoconstriction ICP Blood in brain ICP Progression of S/S of Increasing ICP Mild to moderate Headache, LOC, projectile vomiting, localized pain, decorticate posturing Moderate to severe Pupil changes, hyperventilation, decerebrate posturing, seizures Severe Loss of respiratory control, apnea Progression of S/S of Increasing ICP Severe Respiratory arrest Flaccidity Ischemic response Severe Brain death No spontaneous respirations/3 minutes Fixed pupils Flat EEG Ischemic Response “Cushing’s Reflex” Increased blood pressure Wide pulse pressure Decreased heart rate Loss of respirations Assessment of Brain Function Level of Consciousness: ABCs Manifestations of increased ICP Glasgow Coma Scale headache, vomiting, pupil reactivity Eye Opening Best Motor Response Verbal Response CT scan General Therapy for Increased ICP Elevate HOB Diuretics Sedation Hyperventilation Decompression Classification of Head Injury Concussion Contusion Brainstem Contusion Hemorrhage * Epidural * Subdural - acute - subacute/chronic Intracranial Bleeds epidural bleed skull dura arachnoid subarachnoid bleed subdural bleed CVA: Stroke Thrombotic Embolic atherosclerosis, assess carotids > age 50 atrial fibrillation, valvular disease, hypercoagulable states Hemorrhagic structural anomalies hypertension Stages of Thrombotic Stroke Transient ischemic attacks (TIAs) Stroke in evolution Completed stroke Manifestations of Stroke Acute focal neurological signs may rapidly change (evolve) depends greatly on area of brain damage Transient Ischemic Attack (TIA) signs and symptoms resolve quickly no permanent loss of function Stroke: Ischemic vs Hemorrhagic? TIA: give ASA refer for carotid assessment Stroke: Get CT scan immediately Ischemic: evaluate for tPA (within 3 hours) embolic and thrombotic Hemorrhagic: Neurosurgical consult Chronic Manifestations of Stroke Contralateral hemiplegia Ptosis Homonymous hemianopsia Neglect Aphasia Loss of bowel and bladder control Emotional Instability Homonymous Hemianopsia left visual field right visual field area of stroke damage left visual field blindness General Therapy for CVA Get to a Brain Trauma Center Prevention Manage high blood pressure Anticoagulation Rehabilitation Alzheimer Disease Dementia (deterioration of mentation) about 70% Alzheimer type others are multi-infarct type (vascular) Manifestations (JAMICO) judgment affect Memory Intellect -confusion -orientation Pathology of Alzheimer Disease Genetics VS Environment Apo-E gene toxins, viruses, aluminum Pathological Findings (at autopsy) amyloid plaques neurofibrillary tangles cerebral atrophy and large ventricles Alzheimer Disease Diagnosis of Exclusion MRI rule out other, potentially treatable causes brain atrophy, enlarged ventricles Poor mental function Mini Mental State Exam Seizures Partial Generalized Simple (no LOC) Absence (Petit Mal) Complex ( LOC) Secondarily generalized Tonic-Clonic (Grand Mal) Upper vs Lower Motorneuron UMN LMN Reflexes Increased Decreased Atrophy No Yes Muscle tone Spastic Flaccid Fasciculations No Yes Upper Motor Neuron Disorders Stroke/Head Injury Cerebral Palsy Huntington’s Chorea Parkinson’s Disease Localization of Motor Dysfunction Reflexes Deep tendon reflexes (cord reflexes) Babinski (corticospinal tract) Strength focal vs general ipsilateral vs contralateral spasticity vs flaccidity Parkinson Disease Etiology unknown, possibly neurotoxin – some suspect pesticide exposure – MPTP cases of Parkinson-like syndrome Pathogenesis Low dopamine level in basal ganglia Excessive action of acetylcholine Disease process is progressive Manifestations of Parkinson Disease Classic Triad (unilateral --> bilateral) Akinesia Rigidity Resting tremor Associated Manifestations Propulsive gait Masklike face Drooling - Poor speech quality - 30-50% have dementia Features of Parkinson disease Management of Parkinson Disease Drug Therapy is controversial Restore Dopamine / Ach balance MAOI (selegiline) Amantadine (Symmetrel) Levodopa, carbidopa (Sinemet) anticholinergics (Cogentin, Artane) Surgical Techniques adrenal medulla tissue transplants Brainstem and Spinal Cord Disorders Multiple Sclerosis Poliomyelitis Spinal Cord Injury Multiple Sclerosis Etiology Autoimmune attack on CNS myelin Pathogenesis Immune injury to myelinated neurons Sclerotic plaques noted on MRI Demyelination disturbs neuron conduction Extremely variable course and presentation Presentation of MS Usually relapsing remitting pattern paresthesias gait disturbance leg weakness vision loss (optic neuritis) double vision arm weakness vertigo Diagnosis and Treatment Suspect with episodic neurologic deficits in 20-40 age group especially Northern European MRI lesion is diagnostic Treatment: symptoms Beta interferon may decrease frequency of attacks Immune suppression Transection of Spinal Cord Spinal Shock (lasts 2-8 weeks) loss of spinal cord reflexes below injury – flaccidity – decreased vascular tone - hypotension – atony of bowel and bladder Autonomic Dysreflexia reflex activation of sympathetic neurons below level of injury Autonomic Dysreflexia stimulus (full bladder) Reflex vasoconstriction below level of injury Increased blood pressure Can’t get signal to vessels below injury hypertension x Baroreceptor Response vasodilate above SCI bradycardia Q: What Pattern of Sensory-Motor Impairment Would Occur? transection of lateral cord Contralateral motor? sensory? Ipsilateral motor? sensory? Lower Motor Neuron Disorders Bell’s Palsy Guillian Barre’ Syndrome Guillain Barre’ Syndrome Most common cause of acute flaccid paralysis Presentation: Back leg pain progressing to weakness decreased DTRs Hx viral infection esp. mono preceding decreased nerve conduction velocity Hospitalize, plasmapheresis, IgG Disorder of Neuromuscular Junction Myasthenia Gravis 80%-90% have anti-receptor antibodies 75% have abnormal thymus YY Y Myasthenia Gravis Presentation: NM fatigue which worsens with activity: eye droop, diplopia, head droop, jaw dropping No loss of reflexes, no change in sensation Respond to edrophonium (fast acting anticholinesterase) Muscle Disorders Muscular Dystrophy Disorders of Hearing Conductive hearing loss otosclerosis otitis media Sensorineural hearing loss Presbycusis Menière Disease Disorders of Vision Errors of Refraction myopia, hyperopia, presbyopia Cataract Retinal detachment Glaucoma increased intra-ocular pressure Open Angle Glaucoma fluid Increased anterior chamber IOP clogged canal of Schlemm Closed Angle Glaucoma fluid Increased anterior chamber IOP plugged canal of Schlemm when pupil dilates (acute) Open and Closed Angle Glaucoma Sensory dermatomes Pain Transmission Gate Theory Uses the analogy of a gate to describe how impulses from damaged tissues are sensed in the brain. Pain Transmission, con’t. Tissue injury stimulates the release of: * * * * * Bradykinin Histamine Potassium Prostaglandins Serotonin Pain Transmission, con’t. “A” Fibers * * * * myelin sheath large fiber size conduction is fast inhibits pain transmission * Sharp & welllocalized “C” Fibers * * * * no myelin sheath small fiber size conduction is slow facilitates pain transmission * dull & non-localized Pain Transmission, con’t. Types of pain are related to the proportion of “A” to “C” fibers in the damaged tissue. Pain Transmission, con’t. These two pain fibers enter the spinal cord at the dorsal horn and travel up to the brain. This is the location of the GATE Pain Transmission, con’t. The gates regulate the flow of sensory impulses to the brain! If the gate is closed – no impulses get through. Therefore no impulses are transmitted to the higher centers in the brain so there is no perception of PAIN! Pain Transmission, con’t. It’s the large, activated “A” fibers that closes the gate and this will inhibit transmission to the brain and limits perception of PAIN! Pain Transmission, con’t. It’s the small, activated “C” fibers that opens the gate and this will allows transmission to the brain and causes perception of PAIN! Pain Transmission, con’t. Nerve fibers from the brain innervate the GATE and allow the brain some control over the GATE….in that the brain can: * evaluate the pain * identify the type of pain * localize the pain This also allows the brain to control the GATE before the gate is open. Pain Transmission, con’t. Along with the “A” and “C” fibers, there are specialized cells that control the GATE – these are the “T” cells, which have a threshold…meaning that impulses must overcome the threshold in order to be sent to the brain. Pain Transmission, con’t. Body produces endogenous neurotransmitters: * Enkephalins & Endorphins They are produced by the body to: (1) fight pain (2) bind to opioid receptors (3) inhibit transmission of pain impulses by closing the GATE. Measures to Close the GATE Rubbing the painful area (this inhibits the large “A” sensory fibers Give the opiates to close the GATE (this will reduce recognition of pain) Hang in there – just one more week!!