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NEUROLOGICAL ALTERATIONS

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  1. NEUROLOGICALALTERATIONS NUR 203 Module C

  2. Terms • Define Terms associated with neurological alterations: • Headaches- • Tension, migraines, cluster • Tumors – benign, cancerous • Infections-meningitis, encephalitis • Head injury – contusions, concussions, fractures, intracranial hemorrhage

  3. Terms (cont) • Transient ischemic attacks • Cerebrovascular accidents • Thrombotic • Hemorrhagic • Embolic • Spinal Cord dysfunctions • Spinal cord injuries • Herniated disc

  4. Terms • Spinal Cord dysfunctions • Spinal Shock • Paralysis • Quadriplegic (tetraplegia) • Paraplegic • Autonomic Dysreflexia • Spasticity • Neurogenic bladder/bowel

  5. Terms • Spinal Cord dysfunctions • Respiratory • Sexual • Infection • Neuromuscular dysfunction • Multiple Sclerosis • Parkinson’s • Guillian-Barre • Amyotrophic Lateral Sclerosis

  6. Neuromuscular Dysfunctions • Myasthenia Gravis • Trigeminal Neuralgia • Bell’s Palsy • Muscular Dystrophy • Cerebral Palsy • Neural tube defects

  7. VASCULAR HEADACHES • Tension Headache • Results from muscle contraction • Tight, band-like discomfort that is unrelenting • Pain builds slowly in severity • Triggered by fatigue and stress • Diagnosis confirmed when they occur more than 15 days a month

  8. Treatment: • Stress reduction techniques (bio-feedback, psychotherapy and other methods of stress reduction). Also, correction of poor posture.

  9. Cluster Headaches(sometimes classified as a form of migraine) • Cyclical pattern of periorbital pain lasting form 4 – 8 weeks and usually occurring in the spring or fall • Headache lasts from 15 minutes to hours and may occur several times a day and may awaken from sleep. Unilateral in nature.

  10. Pain is described as deep, boring, intense pain of such severity that the patient has trouble staying still. • May develop Horner’s syndrome • Constricted pupils • Unilateral lacrimation • Rhinorrhea • Triggered by consumption of alcohol • Treated with 100% oxygen via mask • Intranasal Lidocaine may be used

  11. Migraine Headache • Typically a “true vascular headache” • Pain results from vasospasm and ischemia of intracranial vessels. • Unilateral pain, but may alternate sides • Throbbing, pulsatile pain • Photophobia, phonophobia, anorexia, nausea, vomiting and focal neurogenic signs may be present

  12. Aura may precede the event –scintillating scotoma (flashing lights), euphoria, fatigue, yawning, and/or craving for sweets • Can be triggered by relief of intense stress, missing meals, or tyramine rich foods • Patient tries to find relief in a quiet, dark environment • Treatment: avoid precipitating factors • Meds: propranolol, amitriptyline, valporate, verapamil, phenelzine and methysergide taken daily

  13. If medical treatment is sought at the time of the event: • Ergotamine • Dihydroergotamine • Sumatriptan • Chlorpromazine • Prochlorperazine

  14. Patient teaching for migraines: • Identify triggers • Avoid alcohol • Avoid tyramine rich foods • Avoid low blood sugars • Reduce stress

  15. INFECTIOUS / INFLAMMATORY DISORDERS

  16. MENINGITIS • Inflammation of the meninges of the brain and spinal cord • Bacterial • Aseptic (other infective agents—usually viral)

  17. CLINICAL MANIFESTATIONS • Classic symptoms: • Nuchal rigidity • Brudzinski’s sign • Kernig’s sign • Photophobia • Other: fever, tachycardia, h/a, prostration, chills, nausea, vomiting • May be irritable at first with progression to confusion, stupor, and semiconsciousness

  18. Seizures may occur • Petechial or hemorrhagic rash may develop • CSF is cloudy with bacterial

  19. BRUDZINSKI’S SIGN

  20. KERNIG’S SIGN

  21. DIAGNOSIS • Lumbar puncture: • Bacterial: increased protein, decreased glucose, cloudy, increased leukocytes • Viral: increased protein, normal glucose, clear, increased lymphocytes • May culture other areas: blood, wounds, sinuses, etc.

  22. TREATMENT • Isolate until results of CSF analysis are obtained. • Bacterial is very contagious • ABX • Anticonvulsants • Fluid and electrolyte replacement • Monitor for increased ICP • Provide quiet environment • Analgesics may be avoided if they have CNS depressant actions—will mask CNS changes

  23. ENCEPHALITIS • Inflammation of the parenchyma of the brain and spinal cord. Usually caused by a virus. • Arbovirus encephalitis (transmitted by ticks and mosquitoes) • Herpes simplex virus encephalitis may occur as a complication of measles, chickenpox, or mumps.

  24. CLINICAL MANIFESTATIONS • Fever • Headache • Seizures • Nuchal rigidity • Altered LOC • Disorientation • Agitation • Restlessness or lethargy • Drowsiness • Photophobia • N/V

  25. BRAIN ABSCESS • A collection of either encapsulated or free pus within brain tissue arising from a primary focus elsewhere (ear, mastoid process, sinuses, heart, distal bones, lungs, bacteremia, etc).

  26. MANIFESTATIONS • Headache • Lethargy • Drowsiness • Confusion • Depressed mental status • Symptoms of infection • Fever • Chills

  27. Traumatic Brain Injuries • Over 2 million traumatic brain injuries occur each year with approximately 500,000 injuries severe enough to cause hospitalization. • Approximately 50% of all trauma deaths associated with head injury • More than 60% of all vehicular trauma deaths are a result of heat injury

  28. Traumatic Brain Injury -Mechanism of Injury • Penetrating trauma • Blunt trauma • Acceleration • Deceleration • Rotational forces

  29. Traumatic brain Injury – Patho • Primary injury • Secondary injury • Goals of care include efforts to reduce morbidity & mortality from primary & secondary injuries

  30. Traumatic Brain Injury –Patho. – Primary Injury • Occurs at moment of impact • May be mild or severe • Types of primary injuries: • Contusion, laceration, shearing injuries, and hemorrhage

  31. Traumatic Brain Injury –Patho. – Secondary Injury • The biochemical & cellular response to the initial trauma • Can exacerbate the primary injury & cause loss of brain tissue not originally damaged • Ischemia is the primary culprit in secondary brain injury

  32. Traumatic Brain Injury - Patho – Secondary Injury (cont.) • Hypercapnia is a powerful vasodilator • Results in cerebral vasodilatation & increased cerebral blood volume & ICP • Significant hypotension causes inadequate perfusion to neural tissue • *Not typical to be hypotensive with TBI • If hypotensive, need to rule out internal injuries

  33. Traumatic Brain Injury - Patho – Secondary Injury (cont.) • Cerebral edema • Initial hypertension with severe TBI is common • Must control HTN to prevent secondary injury caused by increased ICP • Effects of increases in intracranial pressure may be varied.

  34. BRAIN INJURY –CEREBRAL HEMATOMAS • Extravasation of blood produces a space-occupying lesion on the brain and leads to increased ICP • Epidural & subdural • Extraparenchymal (outside of brain tissue) • Produce injury by pressure effect and displacement of intracranial contents.

  35. Epidural Hematoma • A collection of blood between the inner table of the skull & the outermost layer of the dura • Most often associated with: • Skull fractures • Middle meningeal artery laceration

  36. Epidural Hematoma • Incidence relatively low • Can occur as a result of low-impact injuries (falls) or high-impact injuries (MVAs) • Occurs from trauma to the skull & meninges rather than from the acceleration-deceleration forces seen in other types of head trauma

  37. Epidural Hematoma (cont.) • Clinical manifestations: • Brief loss of consciousness followed by period of lucidity • This lucid period is followed by a rapid deterioration in LOC • Dilated, fixed pupil on the same side as the impact area is a hallmark of EDH • May c/o severe, localized H/A & may be sleepy

  38. Epidural Hematoma (cont.) • Diagnosis: • Based on clinical symptoms & • evidence of a collection of epidural blood identified on CT scan • Treatment: • Involves surgical intervention to remove the blood and to cauterize the bleeding vessels

  39. Subdural Hematoma • The accumulation of blood between the dura and underlying arachnoid membrane. • Most often is related to a rupture in the bridging veins between the brain and the dura. • Acceleration-deceleration & rotational forces are the major causes. • Often associated with cerebral contusions & intracerebral hemorrhage

  40. Subdural Hematoma (cont.) • Three types: • Acute, • subacute, and • chronic • Based on the time frame from injury to clinical symptoms:

  41. Subdural Hematoma - ACUTE • Hematoma that occurs after a severe blow to the head. • Clinical presentation determined by • the severity of injury to the underlying brain at the time of impact & • the rate of blood accumulation in the subdural space.

  42. Subdural Hematoma – ACUTE • Observe for deterioration in level of consciousness or lateralizing signs, • such as inequality of pupils or motor movements. • Deterioration may be rapid • Surgical intervention may include • craniectomy, • craniotomy, or • burr hole evacuation

  43. Subdural Hematoma -SUBACUTE • Develop symptomatically 2 days to 2 weeks after trauma. • Expansion of the hematoma occurs at a rate slower than that in acute SDH. • Takes longer for symptoms to become obvious. • Clinical deterioration with subacute SDH usually is slower than that with acute SDH • Surgical intervention, when appropriate, is the same

  44. Subdural Hematoma – CHRONIC • This term is used when symptoms appear days or months after injury. • Most patients usually are elderly or in late middle age. • Patients at risk include: • Patients with coordination/balance disturbances, • Elderly, • Those receiving anticoagulation therapy

  45. Subdural Hematoma –CHRONIC • Clinical manifestations are insidious • Patient may report a variety of symptoms: • Lethargy, absent-mindedness, headache, vomiting, stiff neck, and photophobia, and show signs of TIA, seizures, pupillary changes, or hemiparesis • Often not seen as initial diagnosis • CT scan can confirm diagnosis of SDH

  46. Subdural Hematoma – CHRONIC • If surgical intervention required, evacuation of the chronic SDH may occur by: • Craniotomy, burr holes, or catheter drainage • Outcome variable • Return of neurologic status variable • Recovery slow • Recurrence frequent

  47. Subarachnoid Hemorrhage (SAH) • Described as bleeding into the subarachnoid space • Usually caused by rupture of a cerebral aneurysm or arteriovenous malformation (AVM). • Accounts for 6% to 7% of all strokes • Non-traumatic SAH affects more than 30,000 people in US each year • Incidence > in women & increases with age

  48. Subarachnoid Hemorrhage (cont.) • Overall mortality rate is 25% with most patients dying on first day after injury. • Approximately 2 million people in the US are believed to have an unruptured cerebral aneurysm, the congenital anomaly responsible for most cases of SAH.

  49. Subarachnoid hemorrhage (cont.) • Known risk factors include: • **Hypertension, • Smoking, • Alcohol use, and • Stimulant use

  50. SAH – Patho • Pathophysiology of two most common causes is distinctly different: • Cerebral Aneurysm • Arteriovenous (AV)Malformation