NEUROPATHOLOGY.ppt

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NEUROPATHOLOGY.ppt

  1. 1. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION CSF pressure is pulsatile at 2 frequencies: *Synchrony with beat by beat change of intracranial blodd volume *Synchrony with respiration (at a slower fre quency as result from changes in intrathora- cic and central venous pressure) </li></ul>
  2. 2. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION(cont) *Normal CSF pressure: -0-140 mm H2O(0-10mmHg=0-1.3kPa) *Intracranial hypertension(ICP): >200 mm H2O (15 mmHg =2kPa) *SLOW elevations up to 200-300 mmH2O (15-22.5 mmHg = 2-3 kPa) may be well tole rated in patients with intracranial expanding lesions </li></ul>
  3. 3. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION(cont) *Values up to and above 500 mmH2O(37.5- 38 mmHg or 5 kPa) are associated with sig nificant cerebral edema *ICP >800 mmH2O (60 mmHg or 8 kPa) is almost always a prelude to death in patients with expanding lesions or head injury </li></ul>
  4. 4. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION(cont) Increased intracranial pressure occurs in 2 main circumstances: 1. Due to the presence of an EXPANDING LESION A.Intracerebral(hemorrhages/hematomas, traumatic or spontaneous; infarction and tumors) B.Meningeal(hemorrhages/hematomas, usually traumatic: extradural, subdural or subarach noidal; tumors vgr. Meningiomas) </li></ul>
  5. 5. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION(cont) Complications of raised ICP: *Reduced cerebral flow -due to reduced cerebral perfusion pressure *Intracranial herniation </li></ul>
  6. 6. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION(cont) Clinical symptoms and signs: -headache -nausea and vomiting -diplopia -papilledema -focal neurologic signs related to intracranial expanding lesions or brain shifts w/herniation -alteration in level of consciousness </li></ul>
  7. 7. NEUROPATHOLOGY <ul><li>CEREBRAL PERFUSION PRESSURE *This is the difference between arterial and intracranial pressure *Compensatory arterial/arteriolar vasodilation mantain cerebral flow AUTOREGULATION -Effective only in conditions of mild to moderate reduction in CPP *CPP =zero= brain death *Intracranial hypertension(CSF pres >200mmH2O and brain edema commonly occur together BUT DO NOT neccesarily coexist </li></ul>
  8. 8. NEUROPATHOLOGY <ul><li>CEREBRAL ISCHEMIC THRESHOLDS Cerebral blood flow(ml./100 g/min) * 50-60 - normal * 20-25 - alteration in level of conscious ness and abnormal EEG *18-20 - isoelectric EEG and neurotransmi tter failure *12-16 – loss of evoked potential and Na+/ K+ pump failure </li></ul>
  9. 9. NEUROPATHOLOGY <ul><li>CEREBRAL ISCHEMIC THRESHOLDS... *10-15 - Ion pump failure and cytogenic (cytotoxic)edema *>10 – Ca++ chanels open, activation of intracellular enzymes and cellular membra ne alterations </li></ul>
  10. 15. NEUROPATHOLOGY <ul><li>CEREBROSPINAL FLUID(CSF) Appearance thin,clear and colorless Coagulation No Blood or RBC No Cell count Mononuclear<5/ml Glucose 60% of serum level Proteins <45 mg/dL </li></ul>
  11. 16. NEUROPATHOLOGY <ul><li>HYDROCEPHALUS *Is the enlargement of the ventricles with increase in the volume of CSF *Usually associated with increased CSF pre ssure *It is required shunting procedures to relieve pressure </li></ul>
  12. 17. NEUROPATHOLOGY <ul><ul><li>CLASSIFICATION: *Communicating(increased production of CSF or decreased absorption by arachnoi dal granulations) *Non-communicating(obstructive),conge nital or acquired *Hydrocephalus ex vacuo </li></ul></ul>
  13. 20. NEUROPATHOLOGY <ul><li>HYDROCEPHALUS...(cont.) CAUSES: *CSF overproduction, vgr. choroid plexus papilloma, Arnold-Chiari malformation *Failure of absorption by arachnoidal granu lations e.g. Post-meningitic leptomeningeal fibrosis, duramater sinus thrombosis, abnor mal arachnoidal granulations. </li></ul>
  14. 21. NEUROPATHOLOGY <ul><li>HYDROCEPHALUS...(cont.) CAUSES... *Congenital stenosis or atresic aqueduct *Obstruction of 3rd ventricle/aqueduct by cysts or neoplasia, gliosis/chronic inflamm. of aqueduct, obstruction of 4th ventricle, or ganized subarachnoidal hemorrhage w/obs truction at the base of encephalus. </li></ul>
  15. 22. NEUROPATHOLOGY <ul><li>HYDROCEPHALUS...(cont.) CAUSES... Compensatory expansion of the ventricles secondary to brain atrophy e.g. Alzheimer´s disease (hydrocephalus ex vacuo) </li></ul>
  16. 24. NEUROPATHOLOGY <ul><li>HYDROCEPHALUS...(cont.) CAUSES... *Obstruction -at level of foramen of Monro-tumors -aqueduct-congenital stenosis,postinflamm., midbrain tumors -4th ventricle-intraventricular,cerebellar and brainstem tumors -foramina of Luschka and Magendie-postmeningitic fibrosis, posterior fossa tumors </li></ul>
  17. 25. NEUROPATHOLOGY <ul><li>HYDROCEPHALUS...(cont.) NORMAL PRESSURE HYDROCEPH. *It is a distinct clinical entity characterized by dementia, gait disturbance and urinary incontinence. *CSF pressure is normal </li></ul>
  18. 26. NEUROPATHOLOGY <ul><li>INTRACRANIAL HYPERTENSION </li></ul><ul><li>*Intracranial hypertension(CSF pressure> 200 mm H2O) and brain edema commonly occur together BUT DO NOT necessarily coexist. </li></ul>
  19. 27. NEUROPATHOLOGY <ul><li>Changes associated w/intracranial expanding lesions: </li></ul><ul><li>*Local deformity </li></ul><ul><li>*Collapse of ventricles -initial spacial compensation by reduction in CSF volume </li></ul><ul><li>*Shift and brain distortion </li></ul><ul><li>*Internal herniations </li></ul>
  20. 28. NEUROPATHOLOGY <ul><li>SULFACINE HERNIATION </li></ul><ul><li>*Herniation under the falx – mainly involving the cingulate gyrus -anterior cerebral artery occlusion leading to infarction of paracentral lobule -spastic paralysis and a cortical sensory disorder in the contralateral leg </li></ul>
  21. 29. NEUROPATHOLOGY <ul><li>SULFACINE HERNIATION...(cont.) *Clinical: *Complications -Headache -Ipsilat.ACA infarct -Contralat.leg if ACA is entrapped weakness under the falx -Assoc.herniation </li></ul>
  22. 34. NEUROPATHOLOGY <ul><li>TRANSTENTORIAL HERNIATION </li></ul><ul><li>*It occurs often as result of shift of supratentorial structures through the incisura tentorii </li></ul><ul><li>*The anatomic structures compressed during the shift include: -ipsilateral oculomotor nerve – pupil dilated with poor or no light reflex </li></ul>
  23. 35. NEUROPATHOLOGY <ul><li>TRANSTENTORIAL HERNIATION... -uncal herniation </li></ul><ul><li>* occlusion of posterior cerebral artery </li></ul><ul><li>* hemorrhagic infarction of temporal and occipital(including calcarine cortex) cortices </li></ul><ul><li>-compression of contralateral cerebral peduncle(Kernohan´s notch) leading to ipsilateral hemorrhage </li></ul>
  24. 44. NEUROPATHOLOGY <ul><li>TRANSTENTORIAL HERNIATION... *Midbrain compression and hemorrhage (Duret) involving midbrain and tegmentum of the pons will produce loss of consciousness and decerebrate rigidity </li></ul>
  25. 45. NEUROPATHOLOGY <ul><li>DESCENDING TRANSTENTORIAL HERNIATION. *Clinical: *Complications: -Ipsilateral dil.pupil -Occipital infarct -Contralateral hemipar. (comp. of ACA) -Ipsilat.hemipar.if there is Kernohan Notch </li></ul>
  26. 46. NEUROPATHOLOGY <ul><li>ASCENDING TRANSTENTORIAL HERNIATION. *Clinical: *Complications: -Nausea -Hydrocephalus -Vomiting -Rapid onset of -Obtundation obtundation  death </li></ul>
  27. 47. NEUROPATHOLOGY <ul><li>FORAMEN MAGNUM(TONSILLAR) HERNIATION. *Associated with expanding supratentorial or infratentorial masses *Characterized by: -cerebellar tonsillar herniation and necrosis -compression of the pyramids  motor signs -compression of RAS  changes in level of consciousness -compression of cardiac/respiratory centers  sudden cardiac/respiratory failure </li></ul>
  28. 51. NEUROPATHOLOGY <ul><li>TONSILLAR HERNIATION... *Clinical: *Complications: -Bilateral arm dysesthes. -Obtundation  -Obtundation death </li></ul><ul><li>*Imagin findings: -Cerebellar tonsils 5 mm below foramen in adults and 7 mm in children </li></ul>

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