• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Pathology of Stroke & CVA
 

Pathology of Stroke & CVA

on

  • 4,387 views

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

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

Statistics

Views

Total Views
4,387
Views on SlideShare
4,379
Embed Views
8

Actions

Likes
1
Downloads
164
Comments
0

3 Embeds 8

http://study.myllps.com 5
https://courses.icc.edu 2
http://docglobal.com 1

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Pathology of Stroke & CVA Pathology of Stroke & CVA Presentation Transcript

    • “The true measure of a man is how he treats someone whodoes him absolutely no good...” – Ann Landers True beauty lies in the Heart….!
    • 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.
    • 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.
    • 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]
    • 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];
    • 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
    • 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
    • Education must award self-confidence, the courage to depend on one’s own strength. - Baba
    • Pathology ofCerebro-Vascular Disease (Stroke) Dr. Shashidhar Venkatesh Murthy Associate Professor & Head of Pathology
    • 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.
    • Introduction:• Stroke is the third most common cause of death and the second most common cause of neurologic disability after Alzheimers 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.
    • 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, 3,5th & 6th layer of cortex, Purkinje cells - cerebellum Border zone (watershed areas) – Brain stem nuclei in infants.
    • Anatomy – Stroke.
    • Brodman’s Cortical Map:
    • 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)
    • 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.
    • Stroke location and incidence: Clinical 30dayCause % presentation mort(%) PathogenesisCerebral 85 Slowly / sudden 15-45 Cerebralinfarction evolving signs and hypoperfusion symptoms Embolism ThrombosisIntracerebral 10 Sudden onset of 80 Rupture of micro-hem. stroke with raised aneurysm or arteriole intracranial pressureSubarachnoid 5 Sudden headache 45 Rupture of saccularhaemorrhage with meningism aneurysm on circle of Willis
    • Hypertensive Intracerebral Hem: Sites 1. Putamen-Claustrum 55% 2. Cerebral white matter 15 3. Thalamus 10 4. Pons 10 5. Cerebellum 10
    • 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.
    • Risk factors:• Non modifiable • Modifiable• Age • Hypertension• Male sex • Diabetes• Race • Smoking• Heredity • Hyperlipidemia • Excess Alcohol* • Heart disease (AF) Oral contraceptives • Hypercoagulability.
    • Clinical Categories:• Global Ischemia. – Hypoxemic encephalopathy – Hypotension, hypoxemia, anemia.• Focal Ischemia. – Obstruction to blood supply to focal area. – Thrombosis, embolism or hemorrhage.
    • 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.
    • Morphology in Global Ischemia1. Watershed zone (Acute - ACA-MCA)2. Laminar necrosis - (chronic- short penetrating arteries)3. Sommer sector of hippocampus.4. Purkinje cells of cerebellum.
    • Watershed/Boundary zone infarcts: Carotid thrombosis
    • Lamellar necrosis in global ischemia. Chronic
    • Local infarction: Cell death ~ 6min central infarct area or umbra, surrounded by a penumbra of ischemic tissue that may recover
    • Infarct Pathogenesis: • Reduced blood supply – hypoxia/anoxia.Hours • Altered metabolism  Na/K pump block. • Glutamate receptor act.  calcium influx. • ischemic injury – Red neuron, vacuolation. • cell death, karyorrhexis.1-day3-day • Inflammation – edema.1 wk. • Macrophages - > 5d. • Liquifaction cavity – >1wk>4wk • Glial proliferation – >1wk. (astrocytes)
    • 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.
    • Cerebral Edema: narrow sulci, flat gyri. Edema -  Normal - 
    • Cerebral edema • Congestion • Flat gyri • Narrow sulci
    • Edema, loss of demarcation:
    • Cerebral Infarct - 2 Weeks
    • Cerebral Infarct – 1-4 Week
    • Cerebral Infarction - Late Cyst + hemosiderin
    • Normal Cerebral cortex:
    • Normal Cerebral cortex: gray matter. Yellow  oligodendrocytes Orange  astrocytes, Blue  neurons.
    • Normal Cerebral cortex: white matter. Yellow  oligodendrocytes Orange  astrocytes
    • Cerebral Edema:Normal Edema
    • Axonal Injury:A, Hypoxic/ischemic injury in cerebral cortex - "red neurons." shrunken cellB, Axonal spheroids at points of axonal disruptionC, Swollen cell body and peripheral dispersion of Nissl substance (chromatolysis)H&E Stain.
    • Acute Infarction: Oedema Edema - Normal
    • Cerebral Infarction: Macrophages
    • Infarct : Microscopy 3 days 1 week >3 week 1 Day DA- 3 days: neutrophils. B-10 days: plenty of macrophagesC-old: tissue loss + gliosis. D-1day: Red neurons & axon bulbs
    • Infarct 4wk - Cyst formation
    • “Where there is love ofMedicine, there is love ofhumankind” -- Hippocrates
    • Specific focal InfarctsMCAACAPCA
    • MCA ACA PCASpecificfocalInfarcts
    • 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.
    • MCA stroke.
    • MCA stroke. Wikipedia: GNU Free Documentation license
    • MCA stroke. Wikipedia: GNU Free Documentation license
    • 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)
    • 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 Wikipedia: GNU Free Documentation license• Urinary incontinence
    • 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
    • Arterial embolic stroke:Embolic stroke: sudden, pin point hemorrhages over a triangular area.
    • Cerebral Infarction – Old (>3w)
    • Cerebral Infarction - Late
    • 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.
    • Hypertension Stroke:Hemorrhagic stroke (new) & Lacunar infarct (old)
    • Ruptured Berry Aneurism
    • Subarachnoid Hemorrhage:
    • Central Pontine Hemorrhage - Herniation
    • Fusiformatherosclerotic aneurysm
    • BerryAneurysm Incidence Pathogenesis
    • Intracerebral Hemorrhage:
    • Intracerebral Hemorrhage:
    • Lacunar Infarct in pons
    • 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 calculatingDiagnosis: Recent cerebral infarction in left MCA distribution.Left cerebral hemisphere shows swelling with compression of the lateralventricle mainly in the frontal area, due to recent infarct in the Middle CerebralArtery (MCA) distribution. The brain in the MCA area shows discoloration ofthe cortex and also blurring between the cortex and white matter.
    • 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
    • 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.
    • 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,
    • Cerebral Infarction: Microscopy Macrophages & Red Neurons Neutrophil Infil. early Gliosis Loss of Myelin Gliosis
    • “The ultimate measure of aman is not where he standsin moments of comfort, but where he stands in time ofchallenge and controversy” – Martin Luther King Jr.
    • A 78y male, hypertensive. Sudden headache collapsedwhile morning walk. Image shows the lesion. Most likelycause?1. Ruptured Berry Aneurysm.2. Ruptured AV malformation.3. Hemorrhagic infarct.4. Lacunar infarct.5. AS- embolic infarct. 55% lesion is a hemorrhagic infarct in the distribution of the RMCA. The basic 35% mechanism is arterial occlusion, usually by an embolus, with reperfusion 8% and leakage through a damaged 2% 0% capillary bed following lysis of the 1 2 3 4 5 embolus.
    • This photograph shows a slice through thecerebral hemispheres. The most likelypathogenesis is:1.Cerebral trauma due to head injury.2.Hypertensive hemorrhage.3.MCA Embolism from a mural thrombosis on a myocardial infarct.4.Atheroma and thrombosis 93% at the carotid bifurcation.5.Bleeding due to Severe thrombocytopenia. 5% 2% 0% 0% 1 2 3 4 5
    • Section of Brain specimen. The lesion is most likely caused by?1. Gunshot2. Coup injury-Contusion3. Contra coup injury.4. Ruptured ACA aneurysm.5. Hypertensive 69% narrowing. 31% 0% 0% 0% 1 2 3 4 5
    • Stroke. Most likely clinical feature?1. Visual deficit.2. Hemiparesis – leg3. Memory deficit. ACA infarct involving the medial and4. Aphasia parasagittal aspect of the motor cortex,5. Emotional disturbance. causing contralateral paralysis of the leg. 65% 30% 4% 0% 0% 1 2 3 4 5
    • This photograph shows a slice through the cerebral hemispheres. The most likely cause is,1. Head injury.2. Hypertensive hemorrhage.3. Embolic infarct.4. Atherosclrerotic narrowing.5. Severe thrombocytopenia. 96% 4% 0% 0% 0% 1 2 3 4 5
    • A 67y man with IHD is rushed to ED after collapse.Brain at autopsy. Most likely Artery involved?1. External Carotid A.2. Internal Carotid A.3. Middle Cerebral A.4. Sagittal venous sinus.5. Anterior Cerebral A. 92% 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 6% deficits. When the dominant hemisphere is0% 0% 2% involved, these lesions are commonly1 2 3 4 5 accompanied by aphasia.
    • Stroke Patient. Most likely Artery involved?1. PCA2. ACA.3. MCA4. Vertebral5. Basilar 96% Infarct involving the ACA distribution. 0% 2% 0% 2% 1 2 3 4 5
    • 28y M, Fever 7d, presents acute hemiparesis & ipsilateral pupillary dilatation. Image cerebellum & pons. ? Diagnosis1. Stroke posterior Cer. Art.2. Bacterial Meningitis.3. Cerebellar Astrocytoma4. Glioblastoma multiforme5. Transtentorial herniation 100% 0% 0% 0% 0% 1 2 3 4 5
    • 85y M, Diabetes, dementia, recent MI, dies of multiorgan failure. Brain at autopsy (aneurysm of PCA) . ? Most common complication1. Dissection.2. Haemorrhage.3. Infection.4. Thrombosis.5. Recanalization. 41% 41% 17% 0% 0% 1 2 3 4 5
    • 78y M, Hypertensive presents with progressive dementia.Image shows section of brain. ? Diagnosis1. Old embolic infarct.2. Hemorrhagic infarct.3. Lacunar infarct4. Recent embolic infarct.5. Atherosclerotic block. 94% 6% 0% 0% 0% 1 2 3 4 5
    • A 72y woman, 1 year history of declining memory developedsudden headache and decreased consciousness andcollapsed while washing dishes. Image shows the lesion.Most likely cause?1. Ruptured Berry Aneurysm.2. Ruptured AV malformation.3. Hemorrhagic infarct.4. Lacunar infarct.5. AS- embolic infarct. 88% 13% 0% 0% 0% 1 2 3 4 5
    • 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).
    • Old & New ACAinfarction 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?
    • Left PCAAtherosclerosiswith old infarctionThis is a view of the cerebral hemispheres after brainstem and cerebellum havebeen removed at the level of the midbrain. There is marked atherosclerosis ofthe left posterior cerebral artery. The left occipital lobe (right side of thephotograph) shows a collapsed pigmented area in the distribution of the posteriorcerebral artery. Diagnosis Atherosclerosis of the left posterior cerebral artery withOld infarction in the area of distribution.Discuss Clinical Presentation? Complications? Cause of death?
    • Recent rightinfarction MCA territory with hemorrhagictransformationAxial view showing (Left: superior section Right: inferior portion). The inferiorportion is through the upper portion of the caudate nuclei and the thalami.The brain shows fragmentation, necrosis, and discoloration in the right MCAdistribution. There is mass effect with compression of the ventricular system. Darkbrown discoloration in the lesion represents early hemorhage.Diagnosis: Recent infarction in the Right MCA territory with hemorrhage.Discuss Clinical Presentation? Complications? Cause of death?
    • Old cystic infarct in the distribution of the left MCACoronal sections of cerebral hemispheres . One is anterior and through the opticchiasm and the posterior section is through the thalami. The left hemisphere (onthe left side of the photograph) is smaller than the right hemisphere. The smallsize of the left hemisphere is due to a large cystic lesion that includes theexternal portion of the putamen, internal capsule, inferior portion of the frontallobe and parts of the temporal lobe. Diagnosis: Old cystic infarct in thedistribution of the left MCA.Discuss Clinical Presentation? Complications? Cause of death?
    • Hypertension:Ruptured anteriorcommunicating or anterior cerebral artery aneurysmCoronal sections of the cerebral hemispheres through the frontal lobesand at the level of the genu of the corpus callosum. A hematoma hasdestroyed the area around the corpus callosum and inferior frontal gyri.Hematoma has ruptured into both lateral ventricles. The location of thehematoma is characteristic of a ruptured anterior communicating oranterior cerebral artery aneurysm due to hypertensionNote: flat gyri, narrow sulci, herniations.Discuss Clinical Presentation? Complications? Cause of death?
    • Spontaneous hypertensive thalamic hemorrhage with intraventricular extensionCoronal section of the cerebral hemispheres through the pulvinar andquadrigeminal plate. The section shows a hematoma that has destroyedpart of the thalamus on the left side. The hematoma has ruptured into thelateral ventricle and has compressed the quadrigeminal plate on the leftside. Diagnosis: Spontaneous hypertensive thalamic hemorrhage withintraventricular extension.Discuss Clinical Presentation? Complications? Cause of death?
    • Spontaneous hypertensivehemorrhage of the left putamenAxial section of the brain through the level of the putamen and the upperportion of the thalami. The left hemisphere shows a localized hematomathat involves the putamen and part of the anterior limb of the internalcapsule. The hematoma has not ruptured into the ventricle and hasspared the insular cortex. Diagnosis: Spontaneous hypertensivehemorrhage of the left putamen.Discuss Clinical Presentation? Complications? Cause of death?
    • Spontaneous hypertensive right cerebellar hemisphere hemorrhage & Acute hydrocephalusThis is an axial section of the brain, brainstem and cerebellum. The section goes through thecaudate nuclei, part of the anterior commissure, the midbrain and the upper portion of thefourth ventricle and cerebellar hemispheres. The brain shows hydrocephalus with dilatation ofboth anterior portions of the lateral ventricles and the temporal horns. The right cerebellarhemisphere is enlarged by a hematoma that has originated near the dentate nucleus and hasdestroyed part of the white matter of the cerebellar hemisphere and the folia.The fourthventricle is compressed to the left side anteriorly. Diagnosis: Spontaneous hypertensive rightcerebellar hemisphere hemorrhage & Acute hydrocephalus.Discuss Clinical Presentation? Complications? Cause of death?
    • Old hypertensive spontaneous hemorrhage left putamenAn axial section of the cerebral hemispheres. Shows a pigmentedslit- like lesion in the left putamen. This pigmentation is rusty brownand within the cavity there is some old blood. The sulci in the insulaare prominent (atrophy). Diagnosis: Old hypertensive spontaneoushemorrhage left putamen.Discuss Clinical Presentation? Complications? Cause of death?
    • 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?
    • Hemorrhagic Cerebral Infarction CT-Scan
    • Cerebral Infarction hemorrhage
    • 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
    • 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 ?
    • “We must all suffer from one of two pains: the pain of discipline or the pain of regret” The difference is painof discipline weighs ounces.. while that of regret weighs ton’s..! Jim Rohn
    • 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
    • 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
    • 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.
    • Occipital Lobe Functions:• Primary visual cortex• Visual association areas• Visual perception• Some visual reflexes (i.e. visual fixation)• Involuntary smooth eye movement
    • 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
    • Motor & Sensory Cortex:
    • Diencephalon & Brain stem:
    • Cranial Nerves:
    • ’Smile’ at each other, smile atyour friends, smile at yourpartner, smile at strangers - itdoesnt matter who it is – Thiswill help you to grow up ingreater love for each other.Mother Teresa1910-1997, Roman Catholic Missionary