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1、Chapter 16：Disease of Central Nervous System,Introduction,1.Delicate structure,more than 50%human genes are neuronal related：complex or arcane2.Lesions may have location indication(selective dysfunction)silent area3.Dual influences of some structures,such as skull and dura,protection of brain and ma
2、y facilitate increased intra-cranial pressure.4.Special disease:degenerative disease,demyelination disease,psychiatric diseases less understanding Congenital anomalies:high incidence,Basic Changes of Cells Neuron（神经元）,Basic Changes of Cells Neuron（神经元）,1.Central Chromatolysis(中央性尼氏小体溶解)Cause：axonal
3、injury,Viral infection,deficiency of Vit.B,anoxia.Morphology:dispersion of the central Nissal substance and swelling of the neuronal body Sequalae:In early stage,increased dissociated ribosome from RER may facilitate protein synthesis.The change would be reversible,if cause abolished.Insistent chang
4、e may lead to neuronal death.,5,Central Chromatolysis,2.Ischemic Changes（Acute Necrosis）Cause：ischemia,anoxia,hypoglucemia,lower blood pressure,epilepsy Morphology：vacuolation,red neuron,Basic Changes of Cells Neuron,7,red neuron,Simple Degeneration(单纯性萎缩）Cause:uncertain,seen in degenerative Dis.Mor
5、phology:neuronal progressive,chronic death,without glial reaction,Basic Changes of Cells Neuron,Neurophagia(嗜神经元现象）dead neuron engulfed and phagocytosed by M.Satellite Phenomenon(卫星现象)more than 5 Oligodendrocytes surrounding one neuron uncertain significance,Basic Changes of Cells Neuron,Inclusion B
6、odies(包涵体)Rabies:Negri body diagnostic hallmark of rabies HSV;Encephalitis B Jap.virus;Poliovirus Parkinson Dis.：Lewy body,Basic Changes of Cells Neuron,11,Rabies,12,Lewy body,Wallerian Degeneration(华勒变性）,Basic Changes of Cells Neuron,Senile Plaque(老年斑)：the core composed with-amyloid protein,surroun
7、ded by a halo and swollen degenerative axons Neurofibrillary Tangle(神经原纤维缠结):the tangle composed by double spiral strands of neurofibils with abnormal phosphorylated tau protein marker of dying neuron seen in Alzheimers Dis.,boxer brain,post-encephalitis,Parkinsonism,Basic Changes of Cells Neuron,15
8、,Senile Plaque,16,Neurofibrillary Tangle,Basic Changes of Cells Astrocyte（星形胶质细胞）,Hypertrophy：The cytoplasm is shown with HE stain.The cell and its nuclei are enlarged with binuclei,multinuclei or bizarre nucleiSeen in local anoxia,edema,infarct and at the periphery of abscess or tumor.Proliferation
9、：reactive:repair process after insults,forming glial scar.Corpora amylacea(淀粉样小体）:with age glycoprotein-rich material,Basic Changes of Cells Oligodendrocyte(少突胶质细胞),Leucodystrophy(白质营养不良)myelin sheath formation disturbance different congenital enzyme deficiency different type of leukodystrophyDemyel
10、ination(脱髓鞘病变)formed myelin sheath destroyed due to allergy,anoxia or toxification,19,Demyelination,20,Demyelination,Ependymal cells(室管膜细胞)Silence,Oncogenesis,Deficiency after injury may repaired by As,forming so called granular ependymitis(颗粒性室管膜炎),Basic Changes of Cells,Microglia(小胶质细胞）Resting mic
11、roglia may activated and turn into M Focal proliferation forming microglial nodule Rodlike microglia seen in advanced syphilis,23,Demyelination,Common Complications脑水肿（Brain Edema),Morphology:brain volume,weight,narrow sulci,widened gyri,cutting surface showed small ventricle,increased reflection.He
12、rniation may ensure.,Common Complications脑水肿（Brain Edema),Increased water contents within brain parenchymaCause:anoxia,infarction,inflammation,injury,toxification and tumor.Mechanism:Vasogenic:disrupted normal BBB,allowing increasing permeability and fluid escaping from vessels into the interstitial
13、 space of brain(interstitial edema)white mattergray matter2.Cytotoxic:cytomembranous pump(ATPase)leading to irons and water accumulation in cells(intracellular edema)white matter=gray matter 3.Usually mixed type,Common complications Hydrocephalus（脑积水),Accumulation of excessive CSF with ventricular d
14、ilatation,27,Over-secretion of CSF(tumor of choroid plexus)Absorption disturbances of CSFNoncomunicating type(obstructive)：obstruction occurs in ventricular system,e.g.tumor,inflammatory,adhesion,hemorrhage,or deformity in III ventricle.Communicating type:obstruction exists in CSF circulation,but ou
15、t of ventricles.It may caused by meningitis,subarachnoid hemorrhage,with subsequent organization,scar fomattion of arachnoid granulation or Villi.,Cause&Pathogenesis,Morphology:Dilation of ventricles with atrophy of parenchyma of brain,due to compression of CSF.CPC:headache,vomiting,edema of papillo
16、edema of optic N.,Common complications Hydrocephalus（脑积水),Common complication,Hypertension of intracranial pressure(ICP)and Herniation(颅内压升高和脑疝形成）The CSF pressure more than 2kPa(normally 0.6-1.8kPa)with lateral recumbent position,Cause：（1）cerebral edema,hydrocephalus（2）occupying lesion:tumor,hemorrh
17、age,hematoma（3）inflammation:meningitis,cerebral abscess,encephalitis（4）brain infarctionThe factors influence the results:（1）the size of the lesion and its development rapidity.（2）existed cranial cavity situationsenile atrophy or unclosure of fontanelle allowing more space for expending of brain,Comm
18、on complications Hypertension of ICP&Herniation,Sequalae：（1）headache,vomiting,papilloedema,coma,death（2）herniationSubfalcine(cingulate gyrus)herniation：local tissue hemorrhagic and necrotic,weakness and sensory dysfunction of leg2)Transtentorial(uncal gyrus)herniation：ipsilateral III N compressed le
19、ading to pupils constricted dilatedKernohan incisionparalysis of ipsilateral extremities(false localization sign)periaquaductal hemorrhageTonsillar herniation,life-threatening press respiration centers in medulla oblongata sudden death,Common complications Hypertension of ICP&Herniation,33,34,Transt
20、entorial(uncal gyrus)herniation,35,Tonsillar herniation,Hemodynamic Derangement&Cerebral Vascular Disorders,Hemodynamic Derangement&Cerebral Vascular Disorders,Circulation disturbances:ischemic encephalopathy infarction(thrombotic or embolitic)hemorrhageVascular disorders:arterosclerosis,atheroscler
21、osis,arteritis,aneurysm,ateriovenous malformation(AVM),Cerebral injury caused by hypertension,cardiac arrest,hemorrhage and shock.Predisposing factors：higher metabolic rate：more susceptible NeuronAsOligoEndo Gray MatterWhite Matter 3rd、5th、6th layers of cortex are most vulnerable,Hemodynamic Derange
22、ment&Cerebral Vascular DisordersIschemic Encephalopathy,Peresistence and severity of ischemia mild ischemia:no remarkable change severe ischemia,survive few hours before death:not remarkable moderate ischemia,survive more than 12 hours：typical changesArchitecture of cerebral arteries the location at
23、 the border zone of cerebral arteries is much more vulnerable.,Hemodynamic Derangement&Cerebral Vascular DisordersIschemic Encephalopathy,40,Changes:laminar cortical necrosis:neurons in 3rd,5th,6th layers of cortex involvedhippocampal sclerosis：pyramidal neuron deathborder zone infarction：early stag
24、e：“C”shaped infarct later stage:astrogliosis(granular atrophy)cardiopetal developmentglobal necrosis(respirator brain)CPC：weakness sensation abnormalities coma,vegetable status death,Hemodynamic Derangement&Cerebral Vascular DisordersIschemic Encephalopathy,Laminar Cortical Necrosis,Hemodynamic Dera
25、ngement&Cerebral Vascular DisordersIschemic Encephalopathy,Fresh border zone infarct,Granular atrophy,Cutting surface of granular atrophy,Respirator brain,Hemodynamic Derangement&Cerebral Vascular DisordersIschemic Encephalopathy,44,Respirator brain,Cause：thrombosis,embolism,space occupying lesion,l
26、ocal vessels compressed by herniaTypes:thrombotic:on the sites of atherosclerosis inner carotid A,basilar A,cerebral arteries,post-communicating A,superior cerebellar A.insidious and gradual development the symptoms:from weakness of muscles to semiplegia or comaembolic:the emboli often are cardiogen
27、ic,or from atherosclerotic plaque,with sudden onset and poor prognosis.,Hemodynamic Derangement&Cerebral Vascular DisordersCerebral Infarction,The most common form of cerebrovascular disease,accounting for 70%80%of all cerebralvascular accidents“stroke”Changes:extent of ischemia:Occlusion in inner c
28、arotid artery:circle willis may compensate completely,no infarctionOcclusion in mid-size artery:as middle cerebral A,the infarct smaller than its supply area due to partial anastomosis.Occlusion in terminal arteries:leading to sudden area infracted.,Hemodynamic Derangement&Cerebral Vascular Disorder
29、sCerebral Infarction,Types:white infarctred infarct:incomplete occlusion or frangible emboli going further to small vessels,resulting in blood escape from injured vascular wall.Morphology changes:first 412h:normal then:ischemic neuronal changes 36-48h:swollen and soft;demarcation between gray and wh
30、ite matter becomes blurred due to edema the third day:macrophage,progressive marked demarcation of the lesion 1 month:liquefaction,irregular cavities 6 month:completely liquefied,Brain infarction,lacunae:necrosis less than 1.5cm in diameter.TIAs(transient ischemic attacks)transient episode of neurol
31、ogic dysfunction lasting several minutes24 hours an important predictor of subsequent infarcts 1/3 patients with TIA developing clinically significant infarcts within 5 years/,Hemodynamic Derangement&Cerebral Vascular DisordersBrain Hemorrhage,Intracerebral HemorrhageCause:hypertension*congenital sa
32、ccular aneurysms,tumors,hemorrhagic diathesis,vasculitis,AVM,traumaPathogenesis:,anoxia of vascular wall,anoxia of perivascular tissue,Charcot Bounchard microaneurysms,micro-softening foci,vessels ruptured,spasm of vessels B.P,hemorrhage,Changes:In the center of foci,normal structure is destroyed an
33、d filled with RBC，at periphery multifoci of hemorrhage The old hemorrhage foci becomes cavitated&with hemosiderin.,Hemodynamic Derangement&Cerebral Vascular DisordersBrain Hemorrhage,CPC：B.G hemorrhage:directed to insular contralateral semiplegia directed to ventricle,thalamus deathPons hemorrhage:p
34、in-like pupils,persistent high fever or sudden deathCerebellar hemorrhage:severe occipital headache,frequent vomiting,Hemodynamic Derangement&Cerebral Vascular DisordersBrain Hemorrhage,Subarachnoid hemorrhage,The most common cause of spontaneous(nontraumatic)Rupture of a saccular(berry)aneurysm app
35、roximately 1%of the general population different from the fusiform dialtion in atheroslcerosis or infectious(mycotic)aneurysm 80%arise at the arterial bifurcations in the territory of the internal carotid artery:MCA,ACMDeveloped the infarct of brain parenchyma,CPC:Abrupt,severe headache,vomitting,lo
36、ss of consciousness Meningeal signs Bloody CSF 50%died in several days acute hydrocephalus herniation brain infarction chronic:hydrocephalus,Vascular malformation,Abnormalities in angiogenesis in the developing brain AVM:the most common caused vessels of variable caliber including A,V Hemorrhagic,ca
37、lcification,reactive gliosis,Tumors of CNSAstrocytoma（星形胶质细胞瘤),The most common categories of brain tumors in CNS Gliomas shares 40%of brain tumors，astrocytoma shares 70%of gliomasMost astrocytomas are of diffuse infiltrativeAstrocytomas in Children and Adults Location differentiation demarcation,oft
38、en in brain stemcerebellum beneathtentorium,well,gelatinousin gross appearance,Children,poor,most often above tentorium in hemispheres,relatively poor granular in gross appearance,well,Adults,Morphology:pilocytic astrocytoma:common in children,elongated processes extend from two poles(grade I)fibril
39、lary astrocytoma and cytoplasmic astrocytoma:minic their original astrocytes(grade II)gemistocytic astrocytoma:(grade IIIII)anaplastic astrocytoma:(grade III)glioblastoma multiform:(grade IV)GFAP(+),Tumors of CNSAstrocytoma（星形胶质细胞瘤),The tumor originates from menigothelium of arachoid granules villa
40、or fibroblasts.Its grows outside the brain,pressing the brain parenchyma and may be resected complete.Grossly:tumor shows spherical or lobulated,expanding in growthHistology:Menigothelial or syncytial type Fibroblastic variants Transitional type OthersPrognosis:most benign,a few(15%)recurs after res
41、ection,few undergoes malignant transformation EMA(+)Vimentin(+),Tumors of CNS Meningioma（脑膜瘤),Embryogenic tumor,malignant,mostly seen in children under ten with poor prognosisThe tumor originates from primitive neuroecdermal cells of vermis or out layers of granular cells of cerebellum.The tumor sho
42、ws whitish pink or gray in color,located at IV ventricle or cerebellar hemisphere.The cells are small,primitive with scanty cytoplasm.The nuclei are round or carrot-shaped with frequent mitoses.Sometimes,may surround a fibrillary core having rosette formationMutual differentiation:GFAP（+）NF（+）,Tumor
43、s of CNS Meduloblastoma（髓母细胞瘤),The benign tumor originates from schwann cell,often located at 8th nerve(acoustic neurilermmoma 听神经瘤）or trunk of peripheral N.Slow growth,very rare malignant transformation Spherical,or lobulated mass,white-gray in color on cut surface,or shows light yellow color when
44、mucinous degeneration occur.quite often cavitation Spindle shaped cells,in whirl or tight arrangement(Antoni A type)or in reticular arrangement（Atoni B型）,Tumors of CNS Schwannoma（神经鞘瘤,施万氏瘤),Etiology the disease cause by living pathogens,which are infective,endemic in certain geographic areas and in
45、certain seasons(传染性，流行性，地方性，季节性）Unique route of invasion,a given pathogen has unique entrance of invasionunique mode of spreading in hostunique affinity for special tissue or organs,causing special pathological changesPathogenesis bacteria:endotoxin and/or exotoxin viruses:cellular and/or humoral im
46、munity,Infectious DiseaseCommon Features(共同特性）,Basic pathologic changes:inflammation(acute/chronic)depending on host pathogen host:immunity pathogen:invasion ability,toxins,metabolic substance evocation of allergic reaction of hostClinical course Incubation period:Predromal period:non specific sympt
47、oms and signs Dominant period:diagnostic symptoms and signs peak Recovery period:the disease subsides typical/atypical/subclinical course,Infectious DiseaseCommon Features(共同特性）,免疫性,ConsequencesComplete recovery the host gains temporary or permanent immunityChronic courseRecurrence of diseaseDeath,I
48、nfectious DiseaseCommon Features(共同特性）,Infectious DiseaseCommon Features in CNS(共同特性）,Meninges dura 硬脑膜 arachnoid 蛛网膜 pia 软脑膜,leptomenige（软脑膜）,Route of infectionHematogenic:septicema,viremiaLocal disseminated:opened skull fracture,sinusitis,mastoiditisDirect infected:trauma,iatrogenic interference(l
49、umbar puncture)Through peripheral nervous system:rabies,HSV,Infectious DiseaseCommon Features in CNS(共同特性）,Inflammation feature,Stereotyped Reaction neurons:degeneration,necrosis secondary demyelination limited exudation with perivascular cuffing formation Presence of BBB(blood brain barrier)and V-R
50、 space limits the spread of inflammation Absence of intrinsic lymphatics and lymphoid tissue T/B cells are blood born(exogenic)glia nodule formation microglial nodule in early stage.astrocytic nodule in later stage,repair,Pathogens:Pyogenic meningitis:Meningococci,H influenza,Pneumococci,Streptococc
