Neurological Pathophysiology

1. Neurological Pathophysiology

2. Edema in the CNS • Increase in tissue mass that results from the excess movement of body fluid from the vascular compartment or its abnormal retention in the tissue. • Why is this a special problem in the brain and spinal cord? • Enclosed space • Lack of lymphatics • Lack of anastomoses in venous drainage

3. Vasogenic edema • Occurs when the blood-brain barrier is upset • Inflammation due to infection • Toxic agents that damage capillary endothelium • Abnormal capillaries associated with malignant neoplasm • Leakage of proteins fluid into interstitium→ swelling • Plasma filtrate accumulation alters ionic balance and impairs function

4. Cytotoxic edema • Intracellular phenomenon • Hypoxia • Cardiac arrest • Near drowning • Strangulation • Focal edema due to blockage of an end artery • Toxic substances that: • Impair sodium/potassium pump • Impair production of ATP

5. In practice, swelling often caused by both • Treatment is different • If swelling is due to cytotoxicity, can give I.V. bolus of a hypertonic solution such as mannitol to draw water into the vasculature and out of the brain • If the cause is vasogenic would this help? • No! would draw fluid into interstitial space and increase swelling!!

6. Increased intracranial pressure (IICP) • Normal intracranial pressure is 5-15 mm Hg • May be due to: • Tumor growth • Edema • Excess cerebrospinal fluid • Hemorrhage

7. Contents of cranium • Tissue of the Central Nervous System • Cerebrospinal Fluid (CSF) • Blood • An increase in any one of these increases intracranial pressure. • Clinical hallmarks of IICP: • Headache • Vomiting • Papilledema – swelling of the optic discs

8. Since the brain is encased in the cranium, the only way pressure can be relieved is by decreasing cranial contents. • Most readily displaced is CSF • If ICP still high, cerebral blood volume is altered: • Stage 1 – vasoconstriction and external compression of the venous system • Compensating, so few symptoms

9. If ICP continues to increase, may exceed brain’s ability to adjust. • Stage 2: • IICP (gradually rising) causes a decrease of oxygenation of neural tissue • Systemic vasoconstriction occurs to increase blood pressure to get blood to brain • Clinical manifestations transient: episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes

10. When ICP begins to = arterial pressure, there is a lack of compensation- beginning decompensation • Stage 3 • Hypoxia and hypercapnia → cytotoxic edema • Decreasing levels of arousal • Widened pulse pressure • May begin Cheynes-Stokes respirations • Bradycardia – due to increased pressure in carotid arteries • Pupils small and sluggish • Surgical or medical intervention needed

11. When all compensatory mechanisms have been exhausted: • Stage 4: • Dramatic rise in ICP in a short time • Autoregulation is lost, and get vasodilation, further increasing intracranial volume • ↓ cerebral perfusion = severe hypoxia and acidosis • Brain contents shift (herniate) from area of high pressure to areas of lower pressure ↓ blood flow

12. Small hemorrhages develop • Ipsilateral pupil dilation and fixation, progressing to bilateral fixed and dilated pupils • When mean systolic arterial pressure equal ICP, cerebral blood flow ceases

13. Treatment • Remove the cause of the IICP • Mechanical hyperventilation to medicated and comatose patient • Reduce blood pressure through diuretics, which slows production of CSF and decreases blood-brain volume • Drugs, us. Barbiturates to slow brain metabolism and ↓ effects of hypoxia • Emergency craniotomy to relieve pressure

15. Brain Trauma • Highest risk: • 15 to 30 years of age • Infants 6 mo. to two years • Young school age children • Elderly persons • Male: female = 3:1

16. Most likely causes of head injury: • Transportation accidents • Falls • Sports related events • Violence

17. Two major categories of head trauma: closed (blunt) trauma open (penetrating) trauma

18. Open (penetrating) trauma Break in dura results in exposure of brain tissues to environment. Results in focal (localized) injury May be due to skull fracture or wound – intracerebral hematoma Traumatic pneumocephalus - injury to a nasal sinus that allows air into brain or ventricles - cerebrospinal rhinorrhea

20. Blunt Head Trauma More common than open trauma. Involves head hitting hard surface or rapidly moving object strikes head Dura is intact – no brain tissue exposed May cause focal or diffuse axonal injury (DAI)

21. Serious injury decrease due to : • Seat belt use • Improved management

22. Mild cerebral concussion • 75- 90 % of all head injuries • Not severe • Diffuse axonal injury – no visible signs on brain • May see transient dizziness, paralysis, unconsciousness, unequal pupils and shock. • Reactive period: vomiting, Temp 99 -100o, rapid pulse, headache, and cerebral irritation lasting 12 -24 hours.

23. Contusions (bruise) : impacts which lead to hemorrhage and possibly hematoma Coup (strike) – head strikes against object shearing forces cause small tears in blood vessels (subdural vessels) edema severity = force smaller area = greater force

24. Contrecoup (rebound) – brain hits opposite side of skull shearing forces and damage opposite to site of impact

26. Extradural (Epidural) Hematomas • 1-2% of major head injuries • Most common in 20-40 year olds • Often caused by temporal skull fracture or injury • Artery is often the source of bleeding • Get herniation (shift) of temporal lobe of brain through tentorial notch

28. Subdural hematomas • 10 - 20 % of persons with traumatic brain injury • Develop rapidly (within hours) • Typically on top of skull • Often due to tearing of veins or dural sinuses • Acts as an expanding mass → IICP→ herniation of brain

29. Intracerebral hematomas • 2-3% of head injuries • Single or multiple • Usually frontal and temporal lobes • May occur in deep white matter • Small blood vessels injured by shearing forces • Acts as expanding mass, compresses tissue, and causes edema • May appear 3- 10 days after head injury

30. Clinical manifestations of contusions • Loss of consciousness, loss of reflexes • Transient cessation of breathing • Brief bradycardia • Decreased blood pressure • As hematoma enlarges: • headache, vomiting, drowsiness, confusion, seizure, hemiparesis

31. Treatment • Contusions: • Control intracranial pressure • Drugs can relieve fluid pressures; may alter Na+ conc. in brain fluids • Manage symptoms • hematomas: • Surgical ligation

32. Cerebrovascular Disease • Most frequent of all neurological problems • Due to blood vessel pathology: • Lesions on walls of vessels leading to brain • Occlusions of vessel lumen by thrombus or embolus • Vessel rupture • Alterations of blood quality

33. CV disease leads to two types of brain abnormalities : Ischemia (with or without infarct) Hemorrhage

34. Cerebrovascular Accident(Stroke) • Clinical expression of cerebrovascular disease: a sudden, nonconvulsive focal neurological deficit • Incidence: third leading cause of death in U.S. – half a million people a year – one third will die from it

35. Incidence • Highest risk > 65 years of age • But about 1/3 (28%) are < 65 years old • Tends to run in families • More often seen in females • More often seen in Blacks, perhaps due to increased incidence of hypertension

36. Three types : • Global hypoperfusion – shock • Ischemia – thrombotic and embolic • Hemorrhagic

37. Risk Factors • Arterial hypertension • Heart disease • Myocardial infarction or endocarditis • Atrial fibrillation • Elevated plasma cholesterol • Diabetes mellitus • Oral contraceptives • Smoking • Polycythemia and thrombocythemia

38. Occlusive strokes • Occurs with blockage of blood vessel by a thrombus or embolus • May be temporary or permanent • Thrombotic stroke: • 3 clinical types: • TIAs • Stroke-in-evolution • Completed stroke

39. Transient Ischemic Attacks • Last for only a few minutes, always less than 24 hours • All neurological deficits resolve • Symptom of developing thrombosis

40. Causes: • Thrombus formation • Atherosclerosis • Arteritis • Hypertension • Vasospasm • Other: • Hypotension • Anemia • Polycythemia

41. Symptoms depend on location • Ophthalmic branch of internal carotid artery – amaurosis fugax – fleeting blindness • Anterior or middle cerebral arteries – contralateral monoparesis, hemiparesis, localized, tingling numbness in one arm, loss of right or left visual field or aphasia

42. Treatment • Without Tx 80% have a recurrence in symptoms, and 1/3 go on to have a full stroke within 5 years • Give anticoagulants prophylactically , usually ½ to 1 aspirin / day

43. Stroke-in-evolution • Can have abrupt onset, but develop in a step-by-step fashion over minutes to hours, occasionally, from days to weeks • Characteristic of thrombotic stroke or slow hemorrhage

44. Thrombotic CVA • Involves permanent damage to brain due to ischemia, hypoxia and necrosis of neurons • Most common form of CVA • Causes: • Atherosclerosis assoc. with hypertension • Diabetes mellitus, and vascular disease • Trauma

45. May take years to develop, often asymptomatic until major narrowing of arterial lumen • Anything that lowers systemic B.P. will exacerbate symptoms (60 % during sleep) • Area affected depends on artery and presence of anastomoses • Area affected initially is greater than damage due to edema • Infarcted tissue undergoes liquifaction necrosis

46. Embolic stroke • Second most common CVA • Fragments that break from a thrombus outside the brain, or occasionally air, fat, clumps of bacteria, or tumors

47. Common causes • Atrial fibrillation • Myocardial infarction • Endocarditis • Rheumatic heart disease and other defects

48. Impact is the same for thrombotic stroke • Rapid onset of symptoms • Often have a second stroke

49. Hemorrhagic Stroke • Third most common, but most lethal • Bleeding into cerebrum or subarachnoid space

50. Causes: • Ruptured aneurysms • Vascular malformations • Hypertension • Bleeding into tumors • Bleeding disorders • Head trauma