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Neurological Disorders

Neurological Disorders. Structural Organization. Cerebral hemispheres. Brainstem & Cerebellum. Spinal and Cranial. Spinal Cord. Nervous System Function. Brain : Central Processing Unit. Sensory Inputs. afferent. efferent. Secretion Movement. anterolateral. dorsal.

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Neurological Disorders

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  1. Neurological Disorders

  2. Structural Organization Cerebral hemispheres Brainstem & Cerebellum Spinal and Cranial Spinal Cord

  3. Nervous System Function Brain: Central Processing Unit Sensory Inputs afferent efferent Secretion Movement

  4. anterolateral dorsal Sensory Tracts

  5. Dorsal column ipsilateral until medulla, then crosses sensation is well localized touch, vibration, pressure, Major Sensory Tracts • Anterolateral (Spinothalamic) • crosses immediately in the cord • sensation is poorly localized • itch, pain, temp

  6. Medial Tracts some tracts cross at medulla, some don’t innervates axial muscles balance, gross motor Major Motor Tracts • Lateral Corticospinal • crosses at medulla • innervates distal muscles • fine motor control

  7. dendrite axon terminal postsynaptic neuron axon synapse How Do Neurons Communicate?

  8. 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)

  9. Head Trauma / Bleeds • Focal: localized • Polar: acceleration-deceleration • Diffuse: widespread disruption

  10. Determinants of Intracranial Pressure • Three space occupying components • Brain • CSF • Blood • Compensation for Increased ICP • CSF shunt to spinal cord • Hyperventilation leading to vasoconstriction

  11. Causes of Increased ICP • Brain infection • Rupture of blood vessels • Hydrocephalus • F & E imbalances • Head Injury – most common

  12. Types of Injury • Primary injury • Secondary injury

  13. Ischemia ATP deficiency Release of glutamate Na+, Ca++ in cell “excitotoxin” Activation of phospholipases mitochondria dysfunction cell damage vasospasm platelet plug free radicals prostaglandins thromboxanes Pathophysiology of Secondary Injury

  14. Compensation for Increased ICP Brain Swelling ICP CSF shunted to spinal cord Hyperventilation PaCO2 CSF in brain ventricles Cerebral vasoconstriction ICP Blood in brain ICP

  15. Mild to moderate Moderate to severe Severe Headache, LOC, projectile vomiting, localized pain, decorticate posturingPupil changes, hyperventilation, decerebrate posturing, seizuresLoss of respiratory control, apnea Progression of S/S of Increasing ICP

  16. Severe Severe Respiratory arrestFlaccidityIschemic responseBrain deathNo spontaneous respirations/3 minutesFixed pupilsFlat EEG Progression of S/S of Increasing ICP

  17. Ischemic Response “Cushing’s Reflex” • Increased blood pressure • Wide pulse pressure • Decreased heart rate • Loss of respirations

  18. Assessment of Brain Function • Level of Consciousness: ABCs • Manifestations of increased ICP • headache, vomiting, pupil reactivity • Glasgow Coma Scale • Eye Opening • Best Motor Response • Verbal Response • CT scan

  19. General Therapy for Increased ICP • Elevate HOB • Diuretics • Sedation • Hyperventilation • Decompression

  20. Classification of Head Injury • Concussion • Contusion • Brainstem Contusion • Hemorrhage * Epidural * Subdural - acute - subacute/chronic

  21. epidural bleed subarachnoid bleed skull subdural bleed dura arachnoid Intracranial Bleeds

  22. CVA: Stroke • Thrombotic • atherosclerosis, assess carotids > age 50 • Embolic • atrial fibrillation, valvular disease, hyper- coagulable states • Hemorrhagic • structural anomalies • hypertension

  23. Stages of Thrombotic Stroke • Transient ischemic attacks (TIAs) • Stroke in evolution • Completed stroke

  24. 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

  25. 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

  26. Chronic Manifestations of Stroke • Contralateral hemiplegia • Ptosis • Homonymous hemianopsia • Neglect • Aphasia • Loss of bowel and bladder control • Emotional Instability

  27. Homonymous Hemianopsia right visual field left visual field area of stroke damage left visual field blindness

  28. General Therapy for CVA • Get to a Brain Trauma Center • Prevention • Manage high blood pressure • Anticoagulation • Rehabilitation

  29. Alzheimer Disease • Dementia (deterioration of mentation) • about 70% Alzheimer type • others are multi-infarct type (vascular) • Manifestations (JAMICO) • judgment -confusion • affect -orientation • Memory • Intellect

  30. 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

  31. Alzheimer Disease • Diagnosis of Exclusion • rule out other, potentially treatable causes • MRI • brain atrophy, enlarged ventricles • Poor mental function • Mini Mental State Exam

  32. Partial Simple (no LOC) Complex ( LOC) Secondarily generalized Generalized Absence (Petit Mal) Tonic-Clonic (Grand Mal) Seizures

  33. Upper vs Lower Motorneuron UMN LMN Reflexes Increased Decreased Atrophy No Yes Muscle tone Spastic Flaccid Fasciculations No Yes

  34. Upper Motor Neuron Disorders • Stroke/Head Injury • Cerebral Palsy • Huntington’s Chorea • Parkinson’s Disease

  35. Localization of Motor Dysfunction • Reflexes • Deep tendon reflexes (cord reflexes) • Babinski (corticospinal tract) • Strength • focal vs general • ipsilateral vs contralateral • spasticity vs flaccidity

  36. 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

  37. Manifestations of Parkinson Disease • Classic Triad (unilateral --> bilateral) • Akinesia • Rigidity • Resting tremor • Associated Manifestations • Propulsive gait - Poor speech quality • Masklike face - 30-50% have dementia • Drooling

  38. Features of Parkinson disease

  39. 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

  40. Brainstem and Spinal Cord Disorders • Multiple Sclerosis • Poliomyelitis • Spinal Cord Injury

  41. 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

  42. Presentation of MS • Usually relapsing remitting pattern • paresthesias • gait disturbance • leg weakness • vision loss (optic neuritis) • double vision • arm weakness • vertigo

  43. 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

  44. 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

  45. Autonomic Dysreflexia stimulus (full bladder) Reflex vasoconstriction below level of injury Increased blood pressure Can’t get signal to vessels below injury x Baroreceptor Response hypertension vasodilate above SCI bradycardia

  46. transection of lateral cord Contralateral motor? sensory? Ipsilateral motor? sensory? Q: What Pattern of Sensory-Motor Impairment Would Occur?

  47. Lower Motor Neuron Disorders • Bell’s PalsyGuillian Barre’ Syndrome

  48. 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

  49. Disorder of Neuromuscular Junction • Myasthenia Gravis • 80%-90% have anti-receptor antibodies • 75% have abnormal thymus Y Y Y

  50. 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)

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