Cerebrovascular diseases 3-rd most common cause of death in developed countries (after cardiovascular diseases and malignant tumors)

Hemodynamic disorders in the CNS IschemicHemorrhagic

Brain ischemia CompleteGlobalRegionalAcuteChronic

Complete ischemia In somatic death Irreversible In the entire brain Connected with ongoing autolysis

Global ischemia In the clinical death In severe heart arythmia In hypotension In shock „Low flow“ states Sequelae: according to duration, condition of the blood vessels, temperature of the body, age, perfusion (reperfusion) pressure, saturation blood with oxygen… Neuronal cell population – most vulnerable, may be different in various part of the brain – cortex, basal ganglia, brain stem Neuronal cell population – most vulnerable, may be different in various part of the brain – cortex, basal ganglia, brain stem Manifestation of infarcts: amnesia, blindness, motoric disrorders, Manifestation of infarcts: amnesia, blindness, motoric disrorders, Global edema – increase of intracranial blood pressure – block of blood perfusion - „coma vigile“, brain death, autolysis – „respirator brain“ Global edema – increase of intracranial blood pressure – block of blood perfusion - „coma vigile“, brain death, autolysis – „respirator brain“

Regional (local) ischemia Brain infarct – „encefalomalacie“ (white, red) Hemispheric – occlusion of internal carotid artery Brain stem – occlusion of vertebral or basilar artery Size of infarct, extension – acc. to site of occlusion, size of stagnating thrombosis, speed of occlusion Mechanism of occlusion – atherosclerosis, embolism, thrombosis (underlined by hypercoagulative conditions, vasculitides, trauma), venous thrombosis – accompanying intracranial inflammations Final result – postnecrotic (postmalatic) pseudocyst

Chronic ischemia Multiple stenoses and occlusions of small arterial branches Brain atrophy: thinning of cortex and gyri, widened sulci, internal hydrocephalus e vacuo, cribose and lacunar status (basal ganglia and centrum semiovale) Status verminosus : multiple small foci of gliosis subsequent to focal necroses of ganglionic cells

Infarcts of spinal cord Much less common than in the brain Local compression – vertebral collumn injuries, disc prolapses into vertebral canal, tumors (primary, secondary) Multiple arterial occlusions – in cases of aortal dissection (thoracal part of spinal cord), multiple embolic occlusion (air embolism…) Morphology – maximum decomposition centromedullary (grey matter)

Intracranial bleeding Traumatic Non traumatic EpiduralSubduralSubarachnoidealIntracerebral

Epidural bleeding (hematoma) Traumatic Arterial (a. meningea media) Usually with skull fracture (very rarely without) Epidural space (intracranially not preformed) Period of latency – hours Development from inicial symptoms to irreversible brain damage - fast (asymmetric compression, herniation, edema, brain death) Requires urgent neurosurgery !!! (anisocoric pupils, mydriasis on the affected size – „surgical pupil“) Fastly killing !!!

Subdural bleeding (hematoma) Both traumatic and „non-traumatic“ Venous (emissarial veins) Not always accompanied by skull fracture Period of latency – long and very variable (even weeks or months) Speed of development from initial symptoms to irreversible brain damage – very variable, may be long Chronic forms: encapsulation, then osmotic expansion (subdural „hygroma“) Needs neurosurgery in the case of clinical symptomatology (may sometimes remain asymptomatic, when stopped early and resolves)

Subarachnoideal bleeding Both traumatic and non-traumatic Traumatic – accompanying brain contusion (combined sources) Non-traumatic – arterial – rupture of berry aneurysm of artery of Willis circle and base of brain Berry aneurysm – inborn predisposition, defects of elastic membranes, can be multiple, then another development due to arterial hypertension and atherosclerosis Site of berry aneurysm: r. communicans ant. 40%, a.cerebri media and it´s branches 34%, a. carotis int. 20% Clinically manifested as acute brain attack Requires neurosurgery (danger of recurrence !!!)

Intracerebral bleeding (hematoma) Usually non traumatic Arterial – arterial hypertension (in the momental rise of intracranial pressure…), usually in the basal ganglia and capsula interna (a. lenticulostriata, „Charcott´s hemorrhagic“ artery), eventually from arteriovenous malformation, arteriovenous hemangioma, cavernous hemangioma, brain metastasis of malignant tumors Complications – brain edema, progression into brain chambers and subarachnoideal space Neurosurgical intervention – considered acc. to circumstances and prognosis… Rare causes: extreme hemorrhagic disorder, vasculitides

Craniocerebral trauma Combination of traumatic changes: Trauma of the skull Vascular trauma with bleeding Trauma of the brain parenchym Opened x closed Traffic injuries, professional injuries, falls from the steps (in drunkness…), falls of objects with hit to the head, shots

Vascular injuries with bleeding See the previously listed types Often combination of types

Parenchymal brain injuries ConcusionContusionLaceration Diffuse axonal damage

Concussion No detectable morphological damage Uncousciousness (very individual duration) Amnesia (always) Desorientation and anxiosity (often)

Contusion More severe trauma, morphological damage (smashing) of brain parenchym Unconsciousness Edema (subsequences…) Always with subarachnoideal and parenchymatous bleeding Coup and contracoup – signs of deceleration of head in movement, under the place of hit, opposite to the place of hit Coup without contracoup (or smaller) – without head movement Life theratening, needs intensive care, neurosurgical consultation

Laceration Usually in penetrating trauma – shot, other severe opened trauma, fatal

Diffuse axonal damage (injury) Angular acceleration of the head - very tangential hit or touch by big power (traffic –car, train…) Multiple mechanical disruption of axons, swelling of their ends Without combination with other type of trauma in about 50% of cases Unconsciousness (usually long duration), desorientation, focal neurological symptoms, Recovery – needs very long time, may be incomplete – posttraumatic dementia in the most severe cases Another morphologic (microscopical) development: proliferation of microglia, degeneration of the involved tracts (different severity from case to case)

Temporal arteritis as an unusual cause of brain infarcts and death (poster congress presentation)