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The central nervous system i

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The central nervous system i

  1. 1. The Central Nervous System
  2. 2. Basic Pathologic Reactions of the CNS
  3. 3. Special Features of the Central Nervous System <ul><li>Complexity of structure and function </li></ul><ul><li>Non-regenerative capacity oft he functional unit - the neuron </li></ul><ul><li>Glial framework rather than fibroblastic </li></ul><ul><li>Concept of blood brain barrier </li></ul>
  4. 4. Special Features of the Central Nervous System <ul><li>Rigid non-expansile framework with limited capacity for about 1600+ gm of matter (brain wt = 1400 gm, blood = 75 mL, total = 150 mL with 75 mL intracranial) </li></ul>
  5. 5. Special Features of the Central Nervous System <ul><li>No classic lymphoid drainage </li></ul><ul><ul><li>A perivascular space system for draining interstitial fluid has been documented </li></ul></ul><ul><li>Exquisite sensitivity to deprivation of oxygen and glucose supply </li></ul>
  6. 6. Blood Brain Barrier <ul><li>Composed of specialized endothelial cells which </li></ul><ul><ul><li>form tight intercellular junctions </li></ul></ul><ul><ul><ul><li>Formation of junctions is dependent on </li></ul></ul></ul><ul><ul><ul><ul><li>Cytokines or factors derived from astrocytes </li></ul></ul></ul></ul><ul><ul><ul><ul><li>The nature of the extracellular matrix </li></ul></ul></ul></ul><ul><ul><li>have few pinocytotic vesicles </li></ul></ul><ul><ul><li>greater number of mitochondria per unit cell than occur in other endothelial cells </li></ul></ul>
  7. 7. Blood Brain Barrier <ul><li>Biochemical features, size, ionization at physiological pH, lipid solubility and extent of binding to plasma proteins influence ability to keep a particular substance out of the brain </li></ul>
  8. 10. Blood Brain Barrier <ul><li>Capillary endothelial cells have specialized mechanisms for control of solute fluxes across the capillary wall which include: </li></ul><ul><ul><li>Differential distribution of membrane pumps between the luminal and antiluminal membranes of endothelial cells </li></ul></ul><ul><ul><li>Have oligosaccharide residues on endothelial luminal plasma membrane compared with those in vessels from other body sites </li></ul></ul><ul><ul><li>The chemical nature of anionic sites on the two membrane surfaces </li></ul></ul>
  9. 11. Alteration or Disruption of Blood Brain Barrier <ul><li>Separation of interendothelial tight junctions or vascular wall disruption </li></ul><ul><li>Injury induced changes in Ca +2 flux and release of polyamines, the effect of which is the </li></ul><ul><ul><li>activation of an increase in endothelial permeability in the form of </li></ul></ul><ul><ul><ul><li>increase in endothelial vesicular transport and carrier mediated membrane transport </li></ul></ul></ul><ul><li>Free radical induced membrane damage leading to </li></ul><ul><ul><li>total disruption of membrane selectivity </li></ul></ul>
  10. 12. Pathology of the Central Nervous System
  11. 13. Cellular Pathology of the Central Nervous System
  12. 14. Reactions of Neurons to Injury
  13. 15. Reactions of Neurons to Injury <ul><li>Acute neuronal injury ( red neuron ) </li></ul><ul><ul><li>Refers to a spectrum of changes that accompany acute CNS hypoxia/ischemia or other acute insults that ultimately lead to death of the cell </li></ul></ul>
  14. 16. Cerebral infarction. A, at low magnification, it is possible to see the demarcated areas of an acute infarction. In the underlying white matter, the areas of infarction are well shown by the myelin stain. B, acute ischemic injury causes diffuse eosinophilia of neurons, which are beginning to shrink. C, infiltration of a cerebral infarct by neutrophils begins at the edges of the lesion where vascular supply has remained intact. D, after about 10 days, an area of infarction is characterized by the presence of macrophages and surrounding reactive gliosis. E, Remote small intracortical infarcts are seen as areas of tissue loss with a small amount of residual gliosis.
  15. 17. Reactions of Neurons to Injury <ul><li>Acute neuronal injury ( red neuron ) </li></ul><ul><ul><li>The morphologic features consist of shrinkage of the cell body, pyknosis of the nucleus, disappearance of nucleolus, and loss of Nissl substance, with intense eosinophilia of the cytoplasm </li></ul></ul>
  16. 18. Reactions of Neurons to Injury <ul><li>Subacute and chronic neuronal injury ( “degeneration” ) </li></ul><ul><ul><li>Refers to situations leading to neuronal death occurring as a result of a progressive disease process of some duration, as is seen in certain slowly evolving neurologic diseases (such as amyotrophic lateral sclerosis) </li></ul></ul>
  17. 19. Reactions of Neurons to Injury <ul><li>Subacute and chronic neuronal injury ( “degeneration” ) </li></ul><ul><ul><li>The characteristic histologic featrure is cell loss, often selectively involving functionally related systems of neurons, and reactive gliosis </li></ul></ul>
  18. 20. Reactions of Neurons to Injury <ul><li>Ferrugination </li></ul><ul><ul><li>Encrustation of neurons with calcium, frequently seen as evidence of remote perinatal or neonatal neuronal hypoxia </li></ul></ul><ul><ul><ul><li>Commonly seen in basal ganglia and thalamus </li></ul></ul></ul>
  19. 21. Reactions of Neurons to Injury <ul><li>Axonal reaction </li></ul><ul><ul><li>Refers to the reaction within the cell body that attends regeneration of the axon </li></ul></ul>
  20. 22. Reactions of Neurons to Injury <ul><li>Axonal reaction </li></ul><ul><ul><li>Morphologic changes visible in the perikaryon include enlargement and rounding up of the cell body, peripheral displacement of the nucleus, enlargement of the nucleolus, and dispersion of Nissl substance from the center to the periphery of the cell ( central chromatolysis ) </li></ul></ul>
  21. 23. Reactions of Neurons to Injury <ul><li>Neuronal damage may be associated with a wide range of subcellular alterations in the neuronal organelles and cytoskeleton </li></ul><ul><ul><li>Neuronal inclusions may occur as a manifestation of aging, when there are intracytoplasmic accumulations of complex lipids ( lipofuscin ), proteins, or carbohydrates </li></ul></ul><ul><ul><ul><li>In these conditions, the neuronal cell body becomes greatly swollen at first because of the intracytoplasmic accumulation of the abnormal metabolite, and the process culminates in death of the cell </li></ul></ul></ul><ul><ul><ul><li>Viral infection can lead to abnormal intranuclear inclusions, as seen in herpetic infection (Cowdry body), cytoplasmic inclusions, as seen in rabies (Negri body), or both nucleus and cytoplasm (cytomegalovirus) </li></ul></ul></ul>
  22. 24. Reactions of Neurons to Injury <ul><li>Some degenerative diseases of the CNS are associated with neuronal intracytoplasmic inclusions, such as neurofibrillary tangles of Alzheimer disease and Lewy bodies of Parkinson disease; others cause abnormal vacuolization of the perikaryon and neuronal cell processes in the neuropil (Creutzfeldt-Jakob disease) </li></ul>
  23. 25. Lewy body: Parkinson’s disease
  24. 26. Hirano body: aging, Alzheimer’s disease
  25. 27. Neurofibrillary tangle
  26. 28. Reactions of Astrocytes to Injury
  27. 29. Reactions of Astrocytes to Injury <ul><li>Gliosis </li></ul><ul><ul><li>The most important histopathologic indicator of CNS injury </li></ul></ul><ul><ul><li>Astrocytes participate in this process by undergoing both hypertrophy and hyperplasia </li></ul></ul><ul><ul><li>Proliferation of astrocytes residing between the molecular and granule cell layers of the cerebellum is a regular accompaniment of anorexic injury and other conditions associated with death of Purkinje cells, termed Bergmann gliosis </li></ul></ul>
  28. 30. Reactions of Astrocytes to Injury <ul><li>Cellular swelling </li></ul><ul><ul><li>Is the swelling of the astrocyte cytoplasm, occurs regularly in acute insults, as in hypoxia, hypoglycemia, and toxic injuries </li></ul></ul>
  29. 31. Reactions of Astrocytes to Injury <ul><li>Rosenthal fibers </li></ul><ul><ul><li>Are thick, elongated, brightly eosinophillic structures that occur within astrocytic processes </li></ul></ul><ul><ul><li>Rosenthal fibers are typically found in regions of long-standing gliosis </li></ul></ul>
  30. 32. Reactions of Astrocytes to Injury <ul><li>Corpora amylacea </li></ul><ul><ul><li>Or polyglucosan bodies, are round, faintly basophilic, periodic acid-Schiff (PAS)-positive, concentrically lamellated structures ranging between 5 and 50 μm in diameter and located wherever there are astrocytic end processes, especially in the subpial and perivascular zones </li></ul></ul><ul><ul><li>They represent a degenerative change in the astrocyte, and they occur in increasing numbers with advancing age and in a rare condition called adult polyglucosan body disease </li></ul></ul>
  31. 33. Reactions of Astrocytes to Injury <ul><li>Glial cytoplasmic inclusions </li></ul><ul><ul><li>Consisting of silver-positive meshes of 20- to 40-nm intermediate filaments that contain the protein α-synuclein are characteristic of a number of CNS degenerative diseases, collectively known as multiple system atrophy </li></ul></ul>
  32. 34. Reactions of Astrocytes to Injury <ul><li>The Alzheimer type II astrocyte </li></ul><ul><ul><li>It is a gray matter astrocyte with a large (two or three times normal) nucleus, pale-staining central chromatin, an intranuclear glycogen droplet, and a prominent nuclear membrane and nucleolus </li></ul></ul><ul><ul><li>It is unrelated to Alzheimer disease </li></ul></ul><ul><ul><ul><li>Rather, it occurs especially in patients with long-standing hyperammonemia due to chronic liver disease, Wilson disease, or hereditary metabolic disorders of the urea cycle </li></ul></ul></ul>
  33. 35. Vascular Reactions
  34. 36. Vascular Reactions <ul><li>Reactive endothelial (vascular) hyperplasia </li></ul><ul><li>Secondary to: </li></ul><ul><ul><li>Vascular infarcts or tissue necrosis induced by other forms of insult </li></ul></ul><ul><ul><li>Tumor induced angiogenesis </li></ul></ul>
  35. 37. Vascular Reactions <ul><li>Arterio(lo)sclerosis - lipohyalinosis </li></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Diabetes </li></ul></ul>
  36. 38. Vascular Reactions <ul><li>Amyloidosis </li></ul><ul><ul><li>Extracellular fibrillar proteins arranged in a β-pleated configuration </li></ul></ul><ul><ul><li>With Congo red stain, amyloid exhibits apple-green birefringence in polarized light </li></ul></ul><ul><ul><li>Vascular involvement leads to congophilic angiopathy and risk of superficial lobar hemorrhage </li></ul></ul>
  37. 39. Cerebral Edema, Raised Intracranial Pressure and Herniation, and Hydrocephalus
  38. 40. Cerebral Edema
  39. 41. Cerebral Edema <ul><li>Cerebral edema or, more precisely, brain parenchymal edema may arise in a setting of a number of diseases -- two principal types are recognized: </li></ul><ul><ul><li>Vasogenic edema occurs when the integrity of the normal blood-brain barrier is disrupted and increased vascular permeability occurs, allowing fluid to escape from the intravascular compartment predominantly into the intercellular spaces of the brain </li></ul></ul>
  40. 42. Cerebral Edema <ul><li>Cerebral edema or, more precisely, brain parenchymal edema may arise in a setting of a number of diseases -- two principal types are recognized: </li></ul><ul><ul><li>Vasogenic edema </li></ul></ul><ul><ul><ul><li>Is the most common form of cerebral edema </li></ul></ul></ul><ul><ul><ul><li>Characterized by incompetence of blood-brain barrier </li></ul></ul></ul><ul><ul><ul><li>High predilection for white matter </li></ul></ul></ul><ul><ul><ul><li>Brain is swollen and soft </li></ul></ul></ul><ul><ul><ul><li>Blurring of gray-white matter junction </li></ul></ul></ul><ul><ul><ul><li>Gyri are flattened and sulci obliterated </li></ul></ul></ul>
  41. 43. Cerebral Edema <ul><li>Cerebral edema or, more precisely, brain parenchymal edema may arise in a setting of a number of diseases -- two principal types are recognized: </li></ul><ul><ul><li>Vasogenic edema </li></ul></ul><ul><ul><ul><li>Spreads by bulk flow rather than by diffusion </li></ul></ul></ul><ul><ul><ul><li>Rate of spread is proportional to capillary hydrostatic pressure </li></ul></ul></ul><ul><ul><ul><li>Seen in the vicinity of brain tumors, intracerebral hematoma, cerebral abscess and contusions </li></ul></ul></ul>
  42. 44. Cerebral Edema <ul><li>Cerebral edema or, more precisely, brain parenchymal edema may arise in a setting of a number of diseases -- two principal types are recognized: </li></ul><ul><ul><li>Cytotoxic edema , in contrast, implies an increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury </li></ul></ul>
  43. 45. Cerebral Edema <ul><li>Cerebral edema or, more precisely, brain parenchymal edema may arise in a setting of a number of diseases -- two principal types are recognized: </li></ul><ul><ul><li>Cytotoxic edema </li></ul></ul><ul><ul><ul><li>Cellular swelling </li></ul></ul></ul><ul><ul><ul><li>Secondary to altered regulation of pump and transport mechanisms for maintenance of cellular homeostasis </li></ul></ul></ul><ul><ul><ul><li>Energy failure is a major cause </li></ul></ul></ul><ul><ul><ul><li>Characteristic of ischemic-encephalopathy </li></ul></ul></ul><ul><ul><ul><li>More prominent in gray matter </li></ul></ul></ul><ul><ul><ul><li>Often occurs concurrently with vasogenic edema </li></ul></ul></ul>
  44. 46. Cerebral Edema <ul><li>In practice, conditions associated with generalized edema oftenn have elements of both vasogenic and cytotoxic edema </li></ul>
  45. 47. Cerebral Edema <ul><li>Interstitial edema (hydrocephalic edema) occurs especially around the lateral ventricles when there is an abnormal flow of fluid from the intraventricular CSF across the ependymal lining to the periventricular white matter in a setting of increased intraventricular pressure </li></ul>
  46. 48. Cerebral Edema <ul><li>Interstitial edema (hydrocephalic edema) </li></ul><ul><ul><li>Increase in water content of periventricular tissue </li></ul></ul><ul><ul><li>Associated with obstructive hydrocephalus </li></ul></ul><ul><ul><li>Water is forced through damaged ependyma into the periventricular tissue </li></ul></ul>
  47. 49. Cerebral Edema <ul><li>The edematous brain is softer than normal and often appears to “overfill” the cranial vault </li></ul><ul><li>In generalized edema, the gyri are flattened, the intervening sulci are narrowed, and the ventricular vacities are compressed </li></ul><ul><li>As the brain expands, herniation may occur </li></ul>Morphology
  48. 50. Cerebral Edema <ul><li>Effects of cerebral edema </li></ul><ul><ul><li>Cerebral ischemia </li></ul></ul><ul><ul><ul><li>Secondary to marked reduction of cerebral perfusion pressure </li></ul></ul></ul><ul><ul><li>Herniation </li></ul></ul><ul><ul><ul><li>Due to raised intracranial pressure and brain shift </li></ul></ul></ul>Morphology
  49. 51. Raised Intracranial Pressure and Herniation
  50. 52. Raised Intracranial Pressure and Herniation <ul><li>Raised intracranial pressure is an increase in mean CSF pressure above 200 mm water with the patient recumbent </li></ul><ul><li>Most cases are associated with a mass effect, either diffuse, as in generalized brain edema, or focal, as with tumors, abscesses, or hemorrhages </li></ul><ul><li>Because the branial vault is subdivided by rigid dural folds (the falx and tentorium), a focal expansion of the brain causes it to be displaced in relation to these partitions </li></ul><ul><ul><li>If the expansion is sufficiently severe, a herniation of the brain will occur </li></ul></ul>
  51. 53. Raised Intracranial Pressure and Herniation <ul><li>Intracranial hypertension </li></ul><ul><ul><li>Is defined as ICP > 200 mm water (15 mm Hg, or 2 kPa) </li></ul></ul><ul><ul><li>Normal range of CSF pressure: </li></ul></ul><ul><ul><ul><li>0 - 140 mm water (0 - 10 mm Hg, 0 - 1.3 kPa) </li></ul></ul></ul><ul><ul><li>Slow elevations up to 200 - 300 mm of water (15 - 22.5 mm Hg, or 2 - 3 kPa) may be well tolerated in patients with intracranial expanding lesions </li></ul></ul>
  52. 54. Raised Intracranial Pressure and Herniation <ul><li>Intracranial hypertension </li></ul><ul><ul><li>Values up to and above 500 mm of water (37.5 - 38 mm Hg, or 5 kPa) are associated with significant cerebral ischemia </li></ul></ul><ul><ul><li>ICP > 800 mm water (60 mm Hg, or 8 kPa) is almost always a prelude to death in patients with expanding lesions and head injury </li></ul></ul>
  53. 55. Raised Intracranial Pressure and Herniation <ul><li>Clinical symptoms and signs of increased ICP </li></ul><ul><ul><li>Headache </li></ul></ul><ul><ul><li>Nausea and vomiting </li></ul></ul><ul><ul><li>Diplopia </li></ul></ul><ul><ul><li>Reduced visual acuity </li></ul></ul><ul><ul><li>Papilledema </li></ul></ul><ul><ul><li>Focal neurologic signs related to intracranial expanding lesions of brain shifts with herniation </li></ul></ul><ul><ul><li>Alteration in level of consciousness </li></ul></ul>
  54. 56. Raised Intracranial Pressure and Herniation <ul><li>Complications of raised ICP </li></ul><ul><ul><li>Reduced cerebral blood flow </li></ul></ul><ul><ul><ul><li>Due to reduced cerebral perfusion pressure </li></ul></ul></ul><ul><ul><li>Intracranial herniation </li></ul></ul>
  55. 57. Major herniations of the brain: subfalcine, transtentorial, and tonsillar
  56. 58. Raised Intracranial Pressure and Herniation <ul><li>Subfalcine (cingulate) herniation </li></ul><ul><ul><li>Occurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx cerebri </li></ul></ul><ul><ul><li>This may be associated with compression of branches of the anterior cerebral artery </li></ul></ul>
  57. 59. Raised Intracranial Pressure and Herniation <ul><li>Transtentorial (uncinate, mesial temporal) herniation </li></ul><ul><ul><li>Occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium cerebelli </li></ul></ul><ul><ul><li>The third cranial nerve is compromised, resulting in pupillary dilation and impairment of ocular movements on the side of the lesion </li></ul></ul><ul><ul><li>The posterior cerebral artery may also be compressed </li></ul></ul>
  58. 60. Duret hemorrhage involving brainstem at the junction of the pons and midbrain
  59. 61. Raised Intracranial Pressure and Herniation <ul><li>Tonsillar herniation </li></ul><ul><ul><li>Reers to displacement of the cerebellar tonsils through the foramen magnum </li></ul></ul><ul><ul><li>This pattern of herniation is life-threatening </li></ul></ul>
  60. 62. Hydrocephalus
  61. 63. Hydrocephalus <ul><li>Hydrocephalus refers to the accumulation of excessive CSF within the ventricular system </li></ul><ul><li>Most cases occur as a consequence of impaired flow and resorption of CSF; in rare instances (e.g., tumors of the choroid plexus), overproduction of CSF may be responsible </li></ul>
  62. 64. Hydrocephalus <ul><li>When hydrocephalus develops before closure of the cranial sutures, there is enlargement of the head, manifested by an increase in head circumference </li></ul>
  63. 65. A, Hydrocephalus. Dilated lateral ventricles seen in a coronal section through the midthalamus.
  64. 66. B, Midsagittal plane T1-weighted magnetic resonance image of a child with communicating hydrocephalus, involving all ventricles.
  65. 67. Trauma
  66. 68. Trauma <ul><li>Injury of several cubic centimeters of brain parenchyma may be clinically silent (e.g., in the frontal lobe), severely disabling (in the spinal cord), or fatal (in the brainstem) </li></ul>
  67. 69. Periventricular leukomalacia. Central focus of white matter necrosis with a peripheral rim of mineralized axonal processes (staining blue)
  68. 70. Trauma <ul><li>The physical forces associated with head injury may result in: </li></ul><ul><ul><li>Skull fractures </li></ul></ul><ul><ul><li>Parenchymal injury </li></ul></ul><ul><ul><li>Vascular injury </li></ul></ul><ul><li>All three can coexist </li></ul>
  69. 71. Skull Fractures
  70. 72. Skull Fractures <ul><li>Fractures that cross sutures are termed diastatic </li></ul><ul><li>When an individual falls while awake, such as might occur when stepping off a ladder, the site of impact is often in the occipital portion of the skull </li></ul><ul><ul><li>In contrast, a fall that follows loss of consciousness, as might follow a syncopal atatack, commonly results in frontal impact </li></ul></ul>
  71. 73. Skull Fractures <ul><li>Symptoms referable to the lower cranial nerves or the cervicomedullary region, and the presence of orbital or mastoid hematomas distant from the point of impact, raise the clinical suspicion of a basal skull fracture </li></ul><ul><li>CSF discharge from the nose or ear and infection (meningitis) may follow </li></ul>
  72. 74. Parenchymal Injuries
  73. 75. Parenchymal Injuries <ul><li>Concussion </li></ul><ul><ul><li>Concussion is a clinical syndrome of alteration of consciousness secondary to head injury typically brought about by a change in the momentum of the head (movement of the head arrested by a rigid surface) </li></ul></ul><ul><ul><li>There is instantaneous onset of transient neurologic dysfunction, including loss of consciousness, temporary respiratory arrest, and loss of reflexes </li></ul></ul><ul><ul><li>Although neurologic recovery is complete, amnesia for the event persists </li></ul></ul><ul><ul><li>Postconcussive neuropsychiatric syndromes are well recognized </li></ul></ul>
  74. 76. Parenchymal Injuries <ul><li>Direct Parenchymal Injury </li></ul><ul><ul><li>Contusion and lasceration are lesions associated with direct parenchymal injury of the brain </li></ul></ul><ul><ul><li>A blow to the surface of the brain, transmitted through the skull, leads to hemorrhage, tissue injury, and edema </li></ul></ul><ul><ul><li>The most common locations where contusions occur correspond to the most frequent sites of direct impact and to regions of the brain that overlie a rough and irregular inner skull surface, such as the frontal lobes along the orbital gyri, and the temporal lobes </li></ul></ul>
  75. 77. Parenchymal Injuries <ul><li>Direct Parenchymal Injury </li></ul><ul><ul><li>Contusions are less frequent over the occipital lobes, brainstem, and cerebellum unless these sites are adjacent to a skull fracture ( fracture contusions ) </li></ul></ul><ul><ul><li>A patient who suffers a blow to the head may develop a cerebral injury at the point of contact (a coup injury) or damage the brain surface diametrically opposite to it (a contrecoup injury) </li></ul></ul><ul><ul><li>Both coup and contrecoup lesions are contusions </li></ul></ul>
  76. 78. Parenchymal Injuries <ul><li>Direct Parenchymal Injury </li></ul><ul><ul><li>Contusions, when seen on cross-section, are wedge-shaped, with the broad base spanning the surface and centered on the point of impact </li></ul></ul>Morphology
  77. 79. A, Multiple contusions involving the inferior surfaces of frontal lobes, anterior temporal lobes, and cerebellum.
  78. 80. B, Acute contusions are present in both temporal lobes, with areas of hemorrhage and tissue disruption
  79. 81. Parenchymal Injuries <ul><li>Direct Parenchymal Injury </li></ul><ul><ul><li>Old traumatic lesions on the surface of the brain have a characteristic macroscopic appearance: they are depressed, retracted, yellowish brown patches involving the crests of gyri most commonly located at the sites of contrecoup lesions (inferior frontal cortex, temporal and occipital poles) </li></ul></ul><ul><ul><ul><li>The term plaque jaune is applied to these lesions, as seen on the inferior frontal surface of the brain in Fig. 28-9C; they can be foci of clinical seizure discharges </li></ul></ul></ul>Morphology
  80. 82. C, Remote contusions are present on the inferior frontal surface of this brain, with a yellow color (associated with the term plaque jaune )
  81. 83. Parenchymal Injuries <ul><li>Direct Parenchymal Injury </li></ul><ul><ul><li>Sudden impacts that result in violent posterior or lateral hyperextension of the neck (as occurs when a pedestrian is struck from the rear by a vehicle) may actually avulse the pons from the medulla or the medulla from the cervical cord, causing instantaneous death </li></ul></ul>
  82. 84. Parenchymal Injuries <ul><li>Diffuse Axonal Injury </li></ul><ul><ul><li>The deep centroaxial white matter regions -- in the supratentorial compartment, particularly the corpus callosum, paraventricular and hippocampal areas and the brainstem along the cerebral peduncles, brachium conjunctivum, superior colliculi, and deep reticular formation -- may also be involved in traumatic injury </li></ul></ul><ul><ul><li>Findings include axonal swelling, indicative of diffuse axonal injury , and focal hemorrhagic lesions </li></ul></ul><ul><ul><ul><li>As many as 50% of patients who develop coma shortly after trauma, even without cerebral contusions, are believed to have white matter damage and diffuse axonal injury </li></ul></ul></ul>
  83. 85. Traumatic Vascular Injury
  84. 86. Traumatic Vascular Injury <ul><li>Vascular injury is a frequent component of CNS trauma and results from direct trauma and disruption of the vessel wall, leading to hemorrhage </li></ul><ul><li>Hemorrhage will occur in any of several compartments (sometimes in combination): epidural , subdural , subarachnoid , and intraparenchymal </li></ul><ul><li>In the cavernous sinus, a traumatic tear of the carotid artery leads to the formation of an arteriovenous fistula </li></ul>
  85. 87. Epidural hematoma (left) in which rupture of meningeal artery, usually associated with a skull fracture, leads to accumulation of arterial blood between the dura and the skull. In a subdural hematoma (right), damage to bridging veins between the brain and the superior sagittal sinus leads to the accumulation of blood between the dura and the arachnoid.
  86. 88. Traumatic Vascular Injury <ul><li>Epidural Hematoma </li></ul><ul><ul><li>Vessels that course within the dura, most importantly the middle meningeal artery, are vulnerable to injury, particularly with skull fractures </li></ul></ul><ul><ul><li>The expanding hematoma has a smooth inner contour that compresses the brain surface </li></ul></ul><ul><ul><li>Clinically, patients can be lucid for several hours between the moment of trauma and the development of neurologic signs </li></ul></ul>
  87. 89. Epidural hematoma covering a portion of the dura. Multiple small contusions are seen in the temporal lobe.
  88. 90. Traumatic Vascular Injury <ul><li>Subdural Hematoma </li></ul><ul><ul><li>Bridging veins travel from the surface of the convexities of the cerebral hemispheres through the subarachnoid space and the subdural space to empty with dural vessels into the superior saggital sinus </li></ul></ul><ul><ul><ul><li>These vessels are the source of bleeding in most cases of subdural hematoma </li></ul></ul></ul>
  89. 91. Traumatic Vascular Injury <ul><li>Subdural Hematoma </li></ul><ul><ul><li>The acute subdural hematoma appears as a collection of freshly clotted blood along the contour of the brain surface, without extension into the depths of sulci </li></ul></ul><ul><ul><li>The underlying brain is flattened, and the subarachnoid space is often clear </li></ul></ul><ul><ul><li>Venous bleeding is self-limited; breakdown and organization of the hematoma take place in time </li></ul></ul>Morphology
  90. 92. Traumatic Vascular Injury <ul><li>Subdural Hematoma </li></ul><ul><ul><li>The organization of subdural hematomas typically occurs in the following sequence: </li></ul></ul><ul><ul><ul><li>Lysis of the clot (about 1 week) </li></ul></ul></ul><ul><ul><ul><li>Growth of fibroblasts from the dural surface into the hematoma (2 weeks) </li></ul></ul></ul><ul><ul><ul><li>Early development of hyalinized connective tissue (1 to 3 months) </li></ul></ul></ul>Morphology
  91. 93. A, Large organizing subdural hematoma attached to the dura. B, Coronal section of the brain showing compression of the hemisphere underlying the hematoma.
  92. 94. Traumatic Vascular Injury <ul><li>Subdural Hematoma </li></ul><ul><ul><li>A common finding in subdural hematomas, however, is the occurrence of multiple episodes of rebleeding ( chronic subdural hematomas ) </li></ul></ul><ul><ul><li>Treatment of subdural hematomas is to remove the organized blood and associated organizing tissue </li></ul></ul>Morphology
  93. 95. Traumatic Vascular Injury <ul><li>Subarachnoid and intraparenchymal hemorrhages most often occur concomitantly in the setting of brain trauma with superficial contusions and lacerations </li></ul><ul><li>Spat-apoplexie (delayed posttraumatic hemorrhage) follows even minor head trauma by an interval of 1 to 2 weeks </li></ul>Morphology
  94. 96. Traumatic Vascular Injury <ul><li>Subdural Hematoma </li></ul><ul><ul><li>Clinical Features </li></ul></ul><ul><ul><ul><li>Subdural hematomas most often become manifest within the first 48 hours after injury </li></ul></ul></ul><ul><ul><ul><li>Neurologic signs commonly observed are attributable to the pressure exerted on the adjacent brain </li></ul></ul></ul><ul><ul><ul><li>The clinical manifestations are nonlocalizing and include headache and confusion </li></ul></ul></ul>
  95. 97. Sequelae of Brain Trauma
  96. 98. Sequelae of Brain Trauma <ul><li>Posttraumatic hydrocephalus is largely due to obstruction of CSF resorption from hemorrhage into the subarachnoid spaces </li></ul><ul><li>Posttraumatic dementia and the punch-drunk syndrome (dementia pugilistica) follow repeated head trauma during a protracted period; the neuropathologic findings include hydrocephalus, thinning of the corpus callosum, difuse axonal injury, neurofibrillary tangles (mainly in the medial temporal areas), and diffuse Aβ-positive plaques </li></ul><ul><li>Other important sequelae of brain trauma include posttraumatic epilepsy, brain tumors (meningioma), infectious diseases, and psychiatric disorders </li></ul>
  97. 99. Spinal Cord Trauma
  98. 100. Spinal Cord Trauma <ul><li>Lesions involving thoracic vertebrae or below can lead to paraplegia </li></ul><ul><li>Cervical lesions result in quadriplegia </li></ul><ul><li>Those above C-4 can, in addition, lead to respiratory compromise from paralysis of the diaphragm </li></ul>
  99. 101. Spinal Cord Trauma <ul><li>At the level of injury, the acute phase consists of hemorrhage, necrosis, and axonal swelling in the surrounding white matter </li></ul>Morphology
  100. 102. Sudden Infant Death Syndrome (SIDS)
  101. 103. Sudden Infant Death Syndrome (SIDS) <ul><li>Definition: Unexpected, sudden infant death which is unexplained after a complete autopsy, scene of death investigation, and review of medical history </li></ul><ul><li>Maternal risk factors: </li></ul><ul><ul><li>Low socioeconomic stats -- decreased age, low education </li></ul></ul><ul><ul><li>Drug use -- e.g., cocaine, heroine, smoking </li></ul></ul>
  102. 104. Sudden Infant Death Syndrome (SIDS) <ul><li>Physical factor -- prone sleep position </li></ul><ul><li>Biological risk factors </li></ul><ul><ul><li>Family history of SIDS </li></ul></ul><ul><ul><li>Apnea of infancy </li></ul></ul><ul><ul><li>Prematurity or fetal growth retardation </li></ul></ul><ul><ul><li>Brain stem dysfunction / immaturity </li></ul></ul>
  103. 105. Sudden Infant Death Syndrome (SIDS) <ul><li>Anatomic and chemoreceptor studies suggest brain stem dysmaturity </li></ul><ul><li>Respiratory control deficit </li></ul><ul><ul><li>Poor chemoreceptor sensitivity </li></ul></ul><ul><ul><ul><li>Diminished responsiveness to hypercarbia and / or hypoxia -- problem with clinical testing is overlap in testing results between normal and at risk infants </li></ul></ul></ul>
  104. 106. Sudden Infant Death Syndrome (SIDS) <ul><li>Deficiency in arousal responsiveness </li></ul><ul><li>General autonomic dysfunction including: </li></ul><ul><ul><li>Deficiency in temperature regulation </li></ul></ul><ul><ul><li>Increased sleep-related sweating </li></ul></ul><ul><ul><li>Alveolar hypoventilation with secondary hypoxia </li></ul></ul>
  105. 107. Credits Books: PBD, 7th Ed. Photos: PBD Interactive Case Study Companion Elsevier Internet: http://www.med.uottawa.ca/patho/neuro/introneuropathology.h tm http://www.radnet.ucla.edu/sections/DINR/Part%2013/Part13A2.h tm

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