patologi anatomy brain and mind system

DEPARTEMEN PATOLOGI ANATOMIFAKULTAS KEDOKTERAN UNIVERSITAS SUMATERA UTARA MEDAN 2013

PNSKumpulan neuron = ganglia CNSKumpulan dari neuron = nuclei **DEP. PATOLOGI ANATOMI FK-USU 2013

DEP. PATOLOGI ANATOMI FK-USU 2013

*DEP. PATOLOGI ANATOMI FK-USU 2013*


BRAIN*DEP. PATOLOGI ANATOMI FK-USU 2013*


Have :Cell bodyDendrites intergrating signalsAxon *DEP. PATOLOGI ANATOMI FK-USU 2013*


Glial divided into :*DEP. PATOLOGI ANATOMI FK-USU 2013*


**DEP. PATOLOGI ANATOMI FK-USU 2013


CELLULAR REACTIONSNeuronsAcute (RED neuron, karyolysis)Subacute, chronic, cell loss, gliosisAxonalInclusions (lipid, prot., carb., viruses)Glia, gliosisSwellingFibersInclusions**DEP. PATOLOGI ANATOMI FK-USU 2013


ACUTE NEURONAL INJURYRED NEURONS**DEP. PATOLOGI ANATOMI FK-USU 2013


**DEP. PATOLOGI ANATOMI FK-USU 2013Hallmark Chronic CNS injuryNeuronal loss &Gliosis


Normal motor units :Two adjacent motor units**DEP. PATOLOGI ANATOMI FK-USU 2013


Abnormal motor units Segmental demyelination:Axon & myocytes remain intact**DEP. PATOLOGI ANATOMI FK-USU 2013Random internodes of myelin are injuredRemyelinated by multiple Schwann cells


Abnormal motor units Axonal degeneration:Resulting :**DEP. PATOLOGI ANATOMI FK-USU 2013Axon & myelin sheath undergo anterograde degeneration (green)Denervation atrophy of the myocytes within its motor unit


Abnormal motor units Reinnervation of muscle:Sprouting of adjacent (red) uninjured motor axons leads to fiber type grouping of myocytes

Injured axon attempts axonal sprouting**DEP. PATOLOGI ANATOMI FK-USU 2013


Abnormal motor units Myopathy :Scattered myocytes of adjacent motor units are small (degenerated / regenerated)

Neurons & nerve fibers are normal**DEP. PATOLOGI ANATOMI FK-USU 2013


PERIPHERAL NERVESame categories of disease as other tissues

The pattern of disease, reflects the unique structure & function of nerves**DEP. PATOLOGI ANATOMI FK-USU 2013


INFLAMMATORY NEUROPATHIESCharacterized by inflammatory cell infiltrates in :Immune mechanisms presumed to be the primary cause of the inflammation**DEP. PATOLOGI ANATOMI FK-USU 2013


Immune-Mediated Neuropathies **DEP. PATOLOGI ANATOMI FK-USU 2013


Is a life-threatening disease PNS**DEP. PATOLOGI ANATOMI FK-USU 2013


Guillain-Barr Syndrome **DEP. PATOLOGI ANATOMI FK-USU 2013


In some patients : **DEP. PATOLOGI ANATOMI FK-USU 2013


INFECTIOUS POLYNEUROPATHIES Many infectious processes affect peripheral nerveCause unique and specific pathologic changes in nerves **DEP. PATOLOGI ANATOMI FK-USU 2013


Biopsies of sural nerves show :**DEP. PATOLOGI ANATOMI FK-USU 2013


Lepromatous & tuberculoid leprosy Peripheral nerveinvolvement in**DEP. PATOLOGI ANATOMI FK-USU 2013


Peripheral nerve involvement**DEP. PATOLOGI ANATOMI FK-USU 2013


Earliest changes seen in :Sensory ganglia

Incomplete blood-nerve barrier allows entry of the toxin

Selective demyelination of axons extends into adjacent anterior & posterior roots (mixed sensorimotor nerves) **DEP. PATOLOGI ANATOMI FK-USU 2013


The most common viral infections of PNS**DEP. PATOLOGI ANATOMI FK-USU 2013


Varicella zoster**DEP. PATOLOGI ANATOMI FK-USU 2013


Classical Disease PatternsDegenerativeInflammatoryNeoplastic**DEP. PATOLOGI ANATOMI FK-USU 2013


Classical CNS Disease PatternsDegenerativeInflammatoryNeoplasticTraumatic**DEP. PATOLOGI ANATOMI FK-USU 2013


CNS MALFORMATIONSNeural TubeAnencephaly, Encephalocele, Spina BifidaForebrainPolymicrogyria, Holoprosencephaly, Agenesis of Corpus CallosumPosterior Fossa (Infratentorial)Arnold Chiari (infratentorial herniation), Dandy-Walker (cerebellar cyst)Syringomyelia/Hydromyelia**DEP. PATOLOGI ANATOMI FK-USU 2013


Fetal -protein in :Amniotic fluid & Maternal circulation**DEP. PATOLOGI ANATOMI FK-USU 2013


SPINABIFIDA**DEP. PATOLOGI ANATOMI FK-USU 2013


POLYMICROGYRIASmall gyri**DEP. PATOLOGI ANATOMI FK-USU 2013


HOLOPROSENCEPHALYFailure prosencephalon to develop, and separate, often leads to cyclops.**DEP. PATOLOGI ANATOMI FK-USU 2013


CEREBRAL EDEMA(Normal weight 1200-1300 grams)**DEP. PATOLOGI ANATOMI FK-USU 2013


Gyrus mendatarSulcus menyempitRongga ventrikel tertekanCEREBRAL EDEMA**DEP. PATOLOGI ANATOMI FK-USU 2013


CEREBRAL EDEMASubfalcine (SUPRA-tentorial)Cingulate (TENTORIAL)Cerebellar tonsilar (SUB-tentorial, or INFRA-tentorial)**DEP. PATOLOGI ANATOMI FK-USU 2013


CEREBRAL EDEMAD.D.:EVERYTHINGSYMPTOMSHEADACHEHALLUCINATIONSCOMADEATH**DEP. PATOLOGI ANATOMI FK-USU 2013


HYDROCEPHALUS**DEP. PATOLOGI ANATOMI FK-USU 2013


HYDROCEPHALUSImpaired RESORPTIONIncreased PRODUCTIONOBSTRUCTIONCOMMUNICATING (entire)NON-COMMUNICATING (part)HIGH PressureNORMAL Pressure**DEP. PATOLOGI ANATOMI FK-USU 2013


PERINATAL Brain InjuriesCerebral Palsy refers to non-progressive diffuse cerebral pathology apparent at childbirthThree most common types of perinatal brain injuriesIntraparenchymal HemorrhageIntraventricular hemorrhage (premies)Periventricular leukomalacia (i.e., infarcts)**DEP. PATOLOGI ANATOMI FK-USU 2013


Various patterns of CNS injury in newborns**DEP. PATOLOGI ANATOMI FK-USU 2013


CNS TRAUMASkull FracturesParenchymal InjuriesTraumatic Vascular InjurySequelaeSpinal Cord Trauma**DEP. PATOLOGI ANATOMI FK-USU 2013


BRAIN TRAUMAContusion (bruise)Laceration (tear)Coup/Contre-CoupConcussion**DEP. PATOLOGI ANATOMI FK-USU 2013


HAIRLINEDEPRESSED, akaDISPLACED**DEP. PATOLOGI ANATOMI FK-USU 2013Skull fracture types


HEMATOMAS/HEMORRHAGEEPIDURAL (fx)SUBDURAL (trauma No fx)SUBARACHNOID (arterial, no trauma)INTRAPARENCHYMAL (any)INTRAVENTRICULAR (no trauma, rare in adults, common in premies)**DEP. PATOLOGI ANATOMI FK-USU 2013


EPIDURAL HEMATOMA**DEP. PATOLOGI ANATOMI FK-USU 2013


SUBDURAL HEMATOMA**DEP. PATOLOGI ANATOMI FK-USU 2013


SUBARACHNOID**DEP. PATOLOGI ANATOMI FK-USU 2013


INTRAPARENCHYMAL**DEP. PATOLOGI ANATOMI FK-USU 2013


Primary Brain Parenchymal Hemorrhage*DEP. PATOLOGI ANATOMI FK-USU 2013*


INTRAVENTRICULAR**DEP. PATOLOGI ANATOMI FK-USU 2013


SPINAL CORD TRAUMAParallels BRAIN patterns of injury on a cellular basisUsually secondary to spinal column displacementLevel of injury mirrors motor loss: Death Quadriplegia Paraplegia**DEP. PATOLOGI ANATOMI FK-USU 2013


Cerebrovascular Diseases (CVA, Stroke)Ischemic ( blood and 02)GlobalFocal (regional): ACUTE: edema neuronal microvacuolization pyknosis karyorrhexis neutrophilsCHRONIC: macrophages gliosis

Hemorrhagic (rupture of artery/aneurysm)**DEP. PATOLOGI ANATOMI FK-USU 2013


HYPERTENSIVE CVAIntracerebralBasal Ganglia Region (lenticulostriate arteries of internal capsule, putamen)**DEP. PATOLOGI ANATOMI FK-USU 2013


HYPERTENSIVE CVA**DEP. PATOLOGI ANATOMI FK-USU 2013


SUBARACHNOIDHEMORRHAGERupture of large intracerebral arteries which are the primary branches of the anatomical circle (of Willis)Congenital (berry aneurysms)Atherosclerotic (atherosclerotic aneurysms, or direct wall rupture)**DEP. PATOLOGI ANATOMI FK-USU 2013


CNS DEGENERATIVE DISEASES**DEP. PATOLOGI ANATOMI FK-USU 2013


CNS DEGENERATIVE DISEASESALZHEIMER DISEASEFrontotemporalPick Disease (also primarily frontal)Progressive Supranuclear Palsy (PSP)CorticoBasal Degeneration (CBD)Vascular Dementias (MID)**DEP. PATOLOGI ANATOMI FK-USU 2013


ALZHEIMER DISEASECommonest cause of dementias (majority)Sporadic, 5-10% familialCORTICAL (grey matter) ATROPHYNEURITIC PLAQUES (extraneuronal)NEUROFIBRILLARY TANGLES (intraneuronal)AMYLOID!!!**DEP. PATOLOGI ANATOMI FK-USU 2013


Normal sulciCortical atrophy**DEP. PATOLOGI ANATOMI FK-USU 2013


Prominent sulci in cortical atrophy. Why are the sulci, NOT the gyri, prominent in atrophy?

Because : cortical LOSS



THANK YOUSELAMAT BELAJAR*DEP. PATOLOGI ANATOMI FK-USU 2013*


*Various glia***Neuronal loss and gliosis is a hallmark of more chronic CNS injury, add to that edema and demyelination.Demyelination = destruction of parts of the myelin sheath covering the nerve*Neuropathies = inflammatory nerve conditions*Plasmapheresis (plasma exchange) is blood purification procedure used to treat several autoimmune disease. It is also known as therapeutic plasma exchange.Plasmapheresis the removal of plasma from withdrawn blood, with retransfusion of the formed elements into the donor; generally, type-specific fresh frozen plasma or albumin is used to replace the withdrawn plasma. The procedure may be done for purposes of collecting plasma components or for the therapeutic purposes. ****COMMON CNS malformations*Anencephaly*Note: the neural canal extends to the outside of the body. Spina bifida occulta is the mildest form of neural tube defect. Characterized by: defective closure of the vertebral arches with intact meninges & spinal cord.Radiograph: may show in 20% of the population.AFP, the same antigen found in hepatomas, is a good screening test for this.*Small gyri*Failure of the prosencephalon to develop, and separate, often leads to cyclops.Cyclopia = Anomali perkembangan yang ditandai dengan fosa orbita tunggal, bola mata (tidak ada / rudimenter / tampak normal / duplikasi), atau hidung tidak ada atau terdapat sebagai sebuah benjolan tubular yang terletak di atas orbita *A comparison of edema compartments the ECS (EXTRA Cellular Space) is vasogenic and the ICS (INTRA Cellular Space) is cytotoxic.*Flattened gyri often signify edema. Why? Ans: compression against the calvarium**1) Falx, 2) Cingulate, and 3) Cereballar tonsillar levels of edema***Basic pathophysiologic concepts about hydrocephalus which is defined as any major deviation from the normal physiology of CSF*Fontanelle closure is the key factor whether hydrocephalus will result in any cranial enlargement*Hydrocephalus, dilated ventricles*These are the three most common types of perinatal brain injuries*Various patterns of CNS injury in newborns, intraventricular bleeding, intraparenchymal bleeding, periventricular infarcts in basal ganglia.*Differentiation between CNS trauma is crucial in medicolegal cases.*Know the correct definitionsContusion = luka memarCoup = pukulan mendadak / tindakan yang cepat dan tepatConcussion = goncangan keras / geger otak*ContusionDo not progressively worsen. *Skull fracture types**Epidural hematoma (left) in which rupture of a meningeal artery, usually associated with a skull fracture, leads to accumulation of arterial blood between the dura and the skull. In a subdural hematoma (right), damage to bridging veins between the brain and the superior sagittal sinus leads to the accumulation of blood between the dura and the arachnoid. **Epidural hematoma covering a portion of the dura. Also present are multiple small contusions in the temporal lobe. (Courtesy of the late Dr. Raymond D. Adams, Massachusetts General Hospital, Boston, MA.) Epidural hematome.The lucid interval is a classic feature of the epidural hematoma. A lucid interval is a periode of time that a person with a head injury is conscious, after being knocked unconscious due to an impact. The interval lasts until they fall unconscious again. Unconsciousness follows a lucid interval because during the interval, blood bluids up on the brain causing extreme pressures on the brain tissue. A lucid interval ends with these pressures becoming so great that the person loses consciousness. They are at great risk of death if medical intervention is not quickly obtained.

*Subdural hematome.No lucid interval, but instead a sudden and progressive worsening of symptoms A, Large organizing subdural hematoma attached to the dura. B, Coronal section of the brain showing compression of the hemisphere underlying the subdural hematoma shown in A. **Primary Brain Parenchymal Hemorrhage

Spontaneous (nontraumatic) intraparenchymal hemorrhages occur most commonly in mid to late adult life, with a peak incidence at about 60 years of age. Most are caused by rupture of a small intraparenchymal vessel. Hypertension is the most common underlying cause, and brain hemorrhage accounts for roughly 15% of deaths among individuals with chronic hypertension. Hypertensive intraparenchymal hemorrhages typically occur in the basal ganglia, thalamus, pons, and cerebellum**You should recall cord injury level versus sensory and motor defects: C5, still alive********FOUR classical areas for brain degeneration, a decent anatomic classification.*ALZHEIMER disease is many times more common than all the other dementias put together.Progressive supranuclear palsy(PSP) is a raredegenerativetauopathy involving the gradual deterioration and death of selected areas of thebrain, chiefly basal ganglia and cortex. CBD is a similar tauopathy. Pick Disease is another tauopathy. Do you see a pattern here?**Normal sulci.*Prominent sulci in cortical atrophy. Why are the sulci, NOT the gyri, prominent in atrophy? Ans: cortical LOSS

patologi anatomy brain and mind system

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