Pathology of Stroke & CVA

Pathology lectures for 4th year medical students on Stroke (Cerebrovascular accident)

1. “The true measure of a man is how he treats someone who does him absolutely no good...” – Ann Landers True beauty lies in the Heart….!

2. CPC 4.3.5 – Robert Robert is a 62 year old recently retired from QLD railways . He lives in Cairns with his wife Rose and their son Aiden who is 40 yrs old with Downs syndrome. He has fallen from a ladder whilst picking mangoes. His wife found him unconscious in the back yard. On arrival at the A&E department he is conscious but appears confused . He is complaining of a pain in his L arm .

3. CPC 4.3.5 – Robert What happened:Patient is unable to talk Collateral History : wife,son, neighbours, paramedics. What happened? Neighbour saw him at top of ladder veer to the left and fall 2.5 m landing on his head . She called out to his wife who attended the scene. Wife says that he did not seem to hear her and his left arm was shaking . The shaking lasted for about 2minutes . He did not seem to regain consciousness until he was administered oxygen by the paramedics about 10 minutes later. He then seemed to come around but appeared confused . He was unable to move his Left arm, R arm and Right leg . Wife says he was well prior to going out to pick mangoes.

4. CPC 4.3.5 – Robert PMH: Hypertension diagnosed in 2000. a bit forgetful taking medication. PSH: 1968 appendicectomy. SH married for 40 years to Rose, they had 2 children . Their oldest Aiden was born with downs syndrome and has lived with them all his life ; alcohol 2 beers x2/week, non smoker. FH mother: breast ca age 72 years ; well age 85yr Father died CVA aged 71 Brother has hypertension and type 2 DM Allergies : aspirin Immunisation Fluvax 4.06, Pneumovax 2004 Medication Ramipril 2.5mg OD [when remembers it]

5. CPC 4.3.5 – Robert T 36.4 C rr 16/min BP 168/98 mmHg pulse 110 bpm irregular , O2 sats RA 92% (on mask O2 4l/min) BMI 31 BGL 16m/mol General appearance : confused to place and time ; no memory of fall or period preceding fall; drooping R side face and R side of body EMST cervical collar ABCDE Peripheries : no clubbing . CRT<2 secs CVS Irregular HR no murmurs , no carotid Bruits CNS GCS 13 Pupils R>L sluggish response[AVPU];

6. CPC 4.3.5 – Robert Boggy Haematoma L temporo parietal area. Gross dysphasia , drooping R side of face , Flaccidity R side of body , brisk reflexes with equivocal plantar reflex Painful swelling with bruising lower L arm just distal to elbow , unable to test L power, tone or reflexes due to pain when moving L arm Power/reflexes/tone normal L leg Sensation : responds to pain Resp., GI, Renal: all normal

7. CPC 4.3.5 – Robert Head injury Contusion, Concussion Epidural hematoma Subdural hematoma Cerebrovascular accident ( stroke ) CVA: embolic CVA: haemorrhagic Metabolic cause Seizure ? cause Trauma to L arm ?# radius / ulna

8. Education must award self-confidence, the courage to depend on one’s own strength. - Baba

9. Pathology of Cerebro-Vascular Disease (Stroke) Dr. Shashidhar Venkatesh Murthy Associate Professor & Head of Pathology

10. Introduction: “ Stroke ” Acute neurological deficit – clinical. Cerebro Vascular accident ( CVA ) – Pathology. Low O2 (hypoxia) / Low blood supply. Varying severity, location & types Transient, evolving & completed. Global / Focal, arterial / venous Ischemic / hemorrhagic.

11. Introduction: Stroke is the third most common cause of death and the second most common cause of neurologic disability after Alzheimer's disease. Its incidence has decreased in recent decades, but the decrease appears now to have leveled off, and it remains the leading cause of institutionalization for loss of independence.

12. Brain Blood Supply Features: High oxygen requirement. Brain 2% of body weight - 15% of cardiac output 20% of total body oxygen Continuous oxygen requirement – no change with BP Few minutes of ischemia - irreversible injury. Neurons - Predominantly aerobic. Sensitive areas: Adults - Hippocampus, 3,5 th & 6 th layer of cortex, Purkinje cells - cerebellum Border zone (watershed areas) Brain stem nuclei in infants.

13. Anatomy – Stroke.

14. Brodman’s Cortical Map:

15. Stroke Types: Clinical Transient Ischemic Attack –TIA - resolve <24h Evolving stroke – increasing >24h. – Thromb. Recurrent / multiple stroke – sec. factors. Completed stroke – no change… embolic. Pathological Focal / Global Ischemic ( Embolic / Thrombotic ), Hemorrhagic . Venous infarcts. (young, infections)

16. Common Types and Incidence: Infarction: Incidence 80% - mortality 40% 50% - Thrombotic – atherosclerosis Large-vessel 30% (carotid, middle cerebral) Small vessel 20% (lacunar stroke) 30% Embolic (heart dis / atherosclerosis) Young, rapid, extensive. Venous thromboembolism (rare) Hemorrhage: Incidence 20% - mortality 80% Berry aneurysm, Microaneurysm, Atheroma. Intracerebral or subarachnoid.

17. Stroke location and incidence: Cause % Clinical presentation 30day mort(%) Pathogenesis Cerebral infarction 85 Slowly / sudden evolving signs and symptoms 15-45 Cerebral hypoperfusion Embolism Thrombosis Intracerebral hem. 10 Sudden onset of stroke with raised intracranial pressure 80 Rupture of micro-aneurysm or arteriole Subarachnoid haemorrhage 5 Sudden headache with meningism 45 Rupture of saccular aneurysm on circle of Willis

18. Hypertensive Intracerebral Hem: Sites 1. Putamen-Claustrum 2. Cerebral white matter 3. Thalamus 4. Pons 5. Cerebellum 55% 15 10 10 10

19. Etiology: Complication of several disorders Atherosclerosis – most common. Hypertension, smoking, diabetes. Heart disease – Atrial fibrillation. Other: Trauma – fat embolism Tumor, Infection Caissons disease – Bends *Pacific.

20. Risk factors: Non modifiable Age Male sex Race Heredity Modifiable Hypertension Diabetes Smoking Hyperlipidemia Excess Alcohol* Heart disease (AF) Oral contraceptives Hypercoagulability.

21. Clinical Categories: Global Ischemia. Hypoxemic encephalopathy Hypotension, hypoxemia, anemia. Focal Ischemia. Obstruction to blood supply to focal area. Thrombosis, embolism or hemorrhage.

22. Global Ischemia: Etiology: Impaired blood supply - Lung & Heart disorders. Impaired O2 carrying – Anemia/Blood dis. Impaired O2 utilization – Cyanide poisoning. Morphology : 3rd, 5th and 6th layers of the cortex, CA1 sector of the hippocampus and in the Purkinje cells in the cerebellum Laminar necrosis, Hippocampus, Purkinje cells. Border zone infarcts – “ Watershed ” Sickle shaped band of necrosis on cortex. Clinical Features : Mild transient confusion state to Severe irreversible brain death. Flat EEG, Vegetative state. Coma.

23. Morphology in Global Ischemia Watershed zone (Acute - ACA-MCA) Laminar necrosis - (chronic- short penetrating arteries) Sommer sector of hippocampus. Purkinje cells of cerebellum.

24. Watershed/Boundary zone infarcts: Carotid thrombosis

25. Lamellar necrosis in global ischemia. Chronic

26. Local infarction: Cell death ~ 6min central infarct area or umbra , surrounded by a penumbra of ischemic tissue that may recover

27. Infarct Pathogenesis: Reduced blood supply – hypoxia/anoxia. Altered metabolism  Na/K pump block. Glutamate receptor act.  calcium influx. ischemic injury – Red neuron, vacuolation. cell death, karyorrhexis. Inflammation – edema. Macrophages - > 5d. Liquifaction cavity – >1wk Glial proliferation – >1wk. (astrocytes) Hours 1-day 3-day 1 wk. >4wk

28. Infarct Stages: Immediate – <24 hours No Change gross, micro  Na/K loss, Ca+ influx. Acute stage – < 1week Oedema , loss of grey/white matter border. Inflammation , Red neurons, necrosis, neutrophils Intermediate stage – 1- 4 weeks. Clear demarcation, soft friable tissue, cysts Macrophages, liquifactive necrosis Late stage – > 4 weeks. Removal of tissue by macrophages Fluid filled cysts with dark grey margin ( gliosis ) Gliosis – proliferation of glia at periphery.

29. Cerebral Edema: narrow sulci, flat gyri. Edema -  Normal - 

30. Cerebral edema Congestion Flat gyri Narrow sulci

31. Edema, loss of demarcation:

32. Cerebral Infarct - 2 Weeks

33. Cerebral Infarct – 1-4 Week

34. Cerebral Infarction - Late Cyst + hemosiderin

35. Normal Cerebral cortex:

36. Normal Cerebral cortex: gray matter . Yellow  oligodendrocytes Orange  astrocytes, Blue  neurons.

37. Normal Cerebral cortex: white matter . Yellow  oligodendrocytes Orange  astrocytes

38. Cerebral Edema: Normal Edema

39. Axonal Injury: A, Hypoxic/ischemic injury in cerebral cortex - "red neurons." shrunken cell B, Axonal spheroids at points of axonal disruption C, Swollen cell body and peripheral dispersion of Nissl substance (chromatolysis) H&E Stain.

40. Acute Infarction: Oedema Edema - Normal

41. Cerebral Infarction: Macrophages

42. Infarct : Microscopy A- 3 days: neutrophils. C-old: tissue loss + gliosis. B-10 days: plenty of macrophages D-1day: Red neurons & axon bulbs D 3 days 1 week >3 week 1 Day

43. Infarct 4wk - Cyst formation

44. “Where there is love of Medicine, there is love of humankind” -- Hippocrates

45. Specific focal Infarcts MCA ACA PCA

46. Specific focal Infarcts MCA ACA PCA

47. MCA Features: Paralysis of the contralateral face, arm and leg Sensory impairment over the contralateral face, arm and leg Homonymous hemi or quadrantonopia Paralysis of gaze to the opposite side Aphasia (dominant) and dysarthria Penetrating - contralateral hemiplegia/paresis, slurred speech.

48. MCA stroke.

49. MCA stroke. Wikipedia: GNU Free Documentation license

50. MCA stroke. Wikipedia: GNU Free Documentation license

51. Major Arteries: MCA MCA Contralateral face & body (arms & leg) paralyasis + Sensory impairment. Homonymous hemi or quadrantonopia. Paralysis of gaze to the opposite side. Aphasia / Apraxia / Agnosia / Dysarthria (dom)

52. ACA stroke. Paralysis of contralateral foot and leg Sensory loss over toes, foot and leg Impairment of gait and stance Abulia (slowness and prolonged delays to perform acts) Flat affect , lack of spontaneity, slowness, distractibility Cognitive impairment , such as perseveration and amnesia Urinary incontinence Wikipedia: GNU Free Documentation license

53. PCA stroke. Peripheral (cortical) Homonymous hemianopia Memory deficits Perseveration (repeat response) Several visual deficits (cortical blindness, lack of depth perception, hallucinations ) Central (penetrating) Thalamus - contralateral sensory loss, spontaneous pain, mild hemi Cerebral peduncle - CN III palsy with contralateral hemiplegia Brain stem - CN palsies, nystagmus, pupillary abnormalities Wikipedia: GNU Free Documentation license

54. Arterial embolic stroke: Embolic stroke: sudden, pin point hemorrhages over a triangular area.

55. Cerebral Infarction – Old (>3w)

56. Cerebral Infarction - Late

57. Hypertensive CVD Intraerebral/Subarachnoid Hemorrhage Microaneurysm hemorrhages – Basal ganglia. Putamen(60%), thalamus, ventricles. Berry aneurysm hemorrhages – subarachnoid. Chronic Hypertension: (dementia) Slit hemorrhages. Microhemorrhages heal as slit with pigment. Lacunar infarcts: Brain stem - pale infarcts. Hypertensive encephalopathy-Malignant. Headache, confusion, vomiting – Raised ICP.

58. Hypertension Stroke: Hemorrhagic stroke (new) & Lacunar infarct (old)

59. Ruptured Berry Aneurism

60. Subarachnoid Hemorrhage:

61. Central Pontine Hemorrhage - Herniation

62. Fusiform atherosclerotic aneurysm

63. Pathogenesis Berry Aneurysm Incidence

64. Intracerebral Hemorrhage:

65. Intracerebral Hemorrhage:

66. Lacunar Infarct in pons

67. Left (Dominant) Hemisphere Stroke: Clinical Aphasia Right hemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze Dysarthria Difficulty reading, writing, or calculating Diagnosis: Recent cerebral infarction in left MCA distribution. Left cerebral hemisphere shows swelling with compression of the lateral ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral Artery (MCA) distribution. The brain in the MCA area shows discoloration of the cortex and also blurring between the cortex and white matter.

68. Right (Non-dominant) - Hemisphere Stroke: Defect of left visual field Extinction of left-sided stimuli Left hemiparesis Left-sided sensory loss Left visual field defect Poor left conjugate gaze Dysarthria Spatial disorientation

69. CNS AV Malformations: Many types: AV Malformation * Cavernous angioma Telangiectasia Venous angioma Cause of Seizure disorders & hemorrhage. Most common congenital vascular malformation. Typically located in the outer cerebral cortex underlying white matter.

70. Summary: Stroke : Ischemic / Thrombotic / Hemorrhagic Acute neurological deficit - Clinical Cerebro Vascular Accident – Pathology. Etiology : Thrombosis, Embolism, Hemorrhage. Risk factors: AS, Hypertension, Smoking. Global – Systemic Hypoxia – Watershed & lamellar infarct Focal – Basal ganglia, Putamen, Int. capsule (MCA) Pathogenesis : Infarction  Liquifaction necrosis  Cyst formation with peripheral gliosis. (loss of neural function) Hypertension & CVA: Atherosclerosis - Thrombosis Haemorrhage (Intra/subarachnoid), chronic benign: Lacunar infarcts & slit hemorrhages. Hypertensive Encephalopathy,

71. Cerebral Infarction: Microscopy Loss of Myelin Red Neurons Neutrophil Infil. Macrophages & early Gliosis Gliosis

72. “The ultimate measure of a man is not where he stands in moments of comfort, but where he stands in time of challenge and controversy” – Martin Luther King Jr.

73. A 78y male, hypertensive. Sudden headache collapsed while morning walk. Image shows the lesion. Most likely cause? Ruptured Berry Aneurysm. Ruptured AV malformation. Hemorrhagic infarct. Lacunar infarct. AS- embolic infarct. lesion is a hemorrhagic infarct in the distribution of the RMCA. The basic mechanism is arterial occlusion, usually by an embolus, with reperfusion and leakage through a damaged capillary bed following lysis of the embolus.

74. This photograph shows a slice through the cerebral hemispheres. The most likely pathogenesis is: Cerebral trauma due to head injury. Hypertensive hemorrhage. MCA Embolism from a mural thrombosis on a myocardial infarct. Atheroma and thrombosis at the carotid bifurcation. Bleeding due to Severe thrombocytopenia.

75. Section of Brain specimen. The lesion is most likely caused by? Gunshot Coup injury-Contusion Contra coup injury. Ruptured ACA aneurysm. Hypertensive narrowing.

76. Stroke. Most likely clinical feature? Visual deficit. Hemiparesis – leg Memory deficit. Aphasia Emotional disturbance. ACA infarct involving the medial and parasagittal aspect of the motor cortex, causing contralateral paralysis of the leg.

77. This photograph shows a slice through the cerebral hemispheres. The most likely cause is, Head injury. Hypertensive hemorrhage. Embolic infarct. Atherosclrerotic narrowing. Severe thrombocytopenia.

78. A 67y man with IHD is rushed to ED after collapse. Brain at autopsy. M ost likely Artery involved? External Carotid A . Internal Carotid A. Middle Cerebral A. Sagittal venous sinus. Anterior Cerebral A. The trifurcation of the middle cerebral artery is a favored site for lodgment of emboli and for thrombosis secondary to atherosclerotic damage. This deprives the parietal cortex of circulation and produces motor and sensory deficits. When the dominant hemisphere is involved, these lesions are commonly accompanied by aphasia.

79. Stroke Patient. Most likely Artery involved? Infarct involving the ACA distribution. PCA ACA . MCA Vertebral Basilar

80. 28y M, Fever 7d, presents acute hemiparesis & ipsilateral pupillary dilatation. Image cerebellum & pons. ? Diagnosis Stroke posterior Cer. Art. Bacterial Meningitis. Cerebellar Astrocytoma Glioblastoma multiforme Transtentorial herniation

81. 85y M, Diabetes, dementia, recent MI, dies of multiorgan failure. Brain at autopsy (aneurysm of PCA) . ? Most common complication Dissection. Haemorrhage. Infection. Thrombosis. Recanalization.

82. 78y M, Hypertensive presents with progressive dementia. Image shows section of brain. ? Diagnosis Old embolic infarct. Hemorrhagic infarct. Lacunar infarct Recent embolic infarct. Atherosclerotic block.

83. A 72y woman, 1 year history of declining memory developed sudden headache and decreased consciousness and collapsed while washing dishes. Image shows the lesion. Most likely cause? Ruptured Berry Aneurysm. Ruptured AV malformation. Hemorrhagic infarct. Lacunar infarct. AS- embolic infarct.

84. Brain Stem Stroke: Common Pattern Pure Motor - Weakness of face and limbs on one side of the body without abnormalities of higher brain function, sensation, or vision (MCA/ACA) Pure Sensory - Decreased sensation of face and limbs on one side of the body without abnormalities of higher brain function, motor function, or vision   (PCA).

85. Old & New ACA infarction Coronal section shows the cerebral hemispheres through the anterior portion of third ventricle, anterior commissure, and the tip of the temporal lobes. This section is not quite symmetrical because it shows more of the anterior portion on the left side. The brain shows a recent area of necrosis in the right anterior cerebral artery distribution near the midline, with fragmentation of the tissue and poorly demarcated cortex and white matter. Corpus callosum is very thin and there is also an old slit-like lesion in the distribution of the left anterior cerebral artery. Diagnosis: Recent infarction in right ACA distribution, and old infarct, left anterior cerebral artery. Discuss Clinical Presentation? Complications? Cause of death? New Old

86. Left PCA Atherosclerosis with old infarction This is a view of the cerebral hemispheres after brainstem and cerebellum have been removed at the level of the midbrain. There is marked atherosclerosis of the left posterior cerebral artery. The left occipital lobe (right side of the photograph) shows a collapsed pigmented area in the distribution of the posterior cerebral artery. Diagnosis Atherosclerosis of the left posterior cerebral artery with Old infarction in the area of distribution. Discuss Clinical Presentation? Complications? Cause of death?

87. Recent right infarction MCA territory with hemorrhagic transformation Axial view showing (Left: superior section Right: inferior portion). The inferior portion is through the upper portion of the caudate nuclei and the thalami. The brain shows fragmentation, necrosis, and discoloration in the right MCA distribution. There is mass effect with compression of the ventricular system. Dark brown discoloration in the lesion represents early hemorhage. Diagnosis: Recent infarction in the Right MCA territory with hemorrhage. Discuss Clinical Presentation? Complications? Cause of death?

88. Old cystic infarct in the distribution of the left MCA Coronal sections of cerebral hemispheres . One is anterior and through the optic chiasm and the posterior section is through the thalami. The left hemisphere (on the left side of the photograph) is smaller than the right hemisphere. The small size of the left hemisphere is due to a large cystic lesion that includes the external portion of the putamen, internal capsule, inferior portion of the frontal lobe and parts of the temporal lobe. Diagnosis: Old cystic infarct in the distribution of the left MCA. Discuss Clinical Presentation? Complications? Cause of death?

89. Hypertension: Ruptured anterior communicating or anterior cerebral artery aneurysm Coronal sections of the cerebral hemispheres through the frontal lobes and at the level of the genu of the corpus callosum. A hematoma has destroyed the area around the corpus callosum and inferior frontal gyri. Hematoma has ruptured into both lateral ventricles. The location of the hematoma is characteristic of a ruptured anterior communicating or anterior cerebral artery aneurysm due to hypertension Note: flat gyri, narrow sulci, herniations. Discuss Clinical Presentation? Complications? Cause of death? A B C

90. Spontaneous hypertensive thalamic hemorrhage with intraventricular extension Coronal section of the cerebral hemispheres through the pulvinar and quadrigeminal plate. The section shows a hematoma that has destroyed part of the thalamus on the left side. The hematoma has ruptured into the lateral ventricle and has compressed the quadrigeminal plate on the left side. Diagnosis: Spontaneous hypertensive thalamic hemorrhage with intraventricular extension. Discuss Clinical Presentation? Complications? Cause of death? A B

91. Spontaneous hypertensive hemorrhage of the left putamen Axial section of the brain through the level of the putamen and the upper portion of the thalami. The left hemisphere shows a localized hematoma that involves the putamen and part of the anterior limb of the internal capsule. The hematoma has not ruptured into the ventricle and has spared the insular cortex. Diagnosis: Spontaneous hypertensive hemorrhage of the left putamen. Discuss Clinical Presentation? Complications? Cause of death?

92. Spontaneous hypertensive right cerebellar hemisphere hemorrhage & Acute hydrocephalus This is an axial section of the brain, brainstem and cerebellum. The section goes through the caudate nuclei, part of the anterior commissure, the midbrain and the upper portion of the fourth ventricle and cerebellar hemispheres. The brain shows hydrocephalus with dilatation of both anterior portions of the lateral ventricles and the temporal horns. The right cerebellar hemisphere is enlarged by a hematoma that has originated near the dentate nucleus and has destroyed part of the white matter of the cerebellar hemisphere and the folia.The fourth ventricle is compressed to the left side anteriorly. Diagnosis: Spontaneous hypertensive right cerebellar hemisphere hemorrhage & Acute hydrocephalus. Discuss Clinical Presentation? Complications? Cause of death?

93. Old hypertensive spontaneous hemorrhage left putamen An axial section of the cerebral hemispheres. Shows a pigmented slit- like lesion in the left putamen. This pigmentation is rusty brown and within the cavity there is some old blood. The sulci in the insula are prominent (atrophy). Diagnosis: Old hypertensive spontaneous hemorrhage left putamen. Discuss Clinical Presentation? Complications? Cause of death? A B

94. Central pontine hemorrhage (  ICP  herniation) This is a transverse section of the pons and cerebellum. The pons is almost completely destroyed by a hematoma that has replaced the tegmentum and most of the basis pontis . The hematoma has ruptured into the fourth ventricle which is obscured by this lesion. The cerebellum is normal . Diagnosis: Central pontine hemorrhage secondary to cerebral herniation – following increased intracranial pressure. Discuss Clinical Presentation? Complications? Cause of death?

95. Hemorrhagic Cerebral Infarction CT-Scan

96. Cerebral Infarction  hemorrhage

97. Brain Stem / Cerebellum / Post Hemisp. Patterns. Motor or sensory loss in all four limbs Crossed signs Limb or gait ataxia Dysarthria Dysconjugate gaze Nystagmus Amnesia Bilateral visual field defects 

98. Investigations: CT of the brain without contrast – location/ext. Electrocardiogram - heart Chest x-ray - heart complete blood count, platelet count – hemat . PT, aPTT – coagulation . Serum electrolytes – complications . Blood glucose - DM Renal and hepatic chemical analyses – status . National Institutes of Health Scale (NIHSS) score – clinical/prognosis ?

99. “We must all suffer from one of two pains: the pain of discipline or the pain of regret” The difference is pain of discipline weighs ounces.. while that of regret weighs ton’s..! Jim Rohn

100. Frontal Lobe Functions: High level cognitive functions. i.e reasoning, abstraction, concentration Storage of information – memory Control of voluntary eye movement Motor control of speech in the dominant hemisphere. Motor Cortex – Motor control of the contralateral side of the body Urinary continence Emotion and personality

101. Parietal Lobe Functions: Sensory cortex – sensory input is interpreted to define size, weight, texture and consistency (contralateral) Sensation is localised, and modalities of touch, pressure and position are identified. Awareness of the parts of body Non-dominant – processes visuospatial information and controls spatial orientation Dominant is involved in ideomotor praxis (ability to perform learned motor tasks

102. Temporal Lobe Functions: Primary auditory receptive areas In dominant ability to comprehend speech (wernicke’s) – reception Interpretive area – area at the junction of the temporal, parietal and occipital lobes. Plays an important role in visual, auditory and olfactory perception Important role in learning; memory and emotional affect.

103. Occipital Lobe Functions: Primary visual cortex Visual association areas Visual perception Some visual reflexes (i.e. visual fixation) Involuntary smooth eye movement

104. Diencephalon Functions: Brain Stem: Midbrain, Pons & Medulla 10 of the 12 ranial nerves arise from the brainstem ( ipsilateral signs) Cortical pathway decussation contralateral signs. Some major functions: eye movement, swallowing, breathing, blood pressure, heat beat, consciousness Cerebellum: movement – Balance & coordination

105. Motor & Sensory Cortex:

106. Diencephalon & Brain stem:

107. Cranial Nerves:

108. ’Smile’ at each other, smile at your friends, smile at your partner, smile at strangers - it doesn't matter who it is – This will help you to grow up in greater love for each other. Mother Teresa 1910-1997, Roman Catholic Missionary