CNS Traumatic & Non-traumatic Injury 2024 PDF

Traumatic & Non-traumatic Injury of the central nervous system Dr Wan Syahira Ellani Wan Ahmad Kammal Anatomic Pathologist Dept of Pathology, FPSK [email protected]  LEARNING OBJECTIVES 1)To describe and identify the definition and sites of traumatic brain injury including...

Traumatic & Non-traumatic Injury of the central nervous system Dr Wan Syahira Ellani Wan Ahmad Kammal Anatomic Pathologist Dept of Pathology, FPSK [email protected]  LEARNING OBJECTIVES 1)To describe and identify the definition and sites of traumatic brain injury including the pathogenesis, morphological features and sequalae. 2) To describe and identify the definition and classification of non-traumatic brain injury including the pathogenesis and morphological features.  LECTURE CONTENT Traumatic head injury 1) Skull fractures 2) Traumatic parenchymal injury 3) Traumatic vascular injury a) Epidural haemorrhage b) Subdural haemorrhage c) Subarachnoid haemorrhage d) Intraparenchymal haemorrhage 4) Sequelae of brain trauma Non-traumatic brain injury o Haemorrhagic stroke o Subarachnoid haemorrhage o Intraparenchymal haemorrhage o Ischaemic stroke (Focal/ Global) o Hypertensive cerebrovascular disease  TRAUMATIC HEAD INJURY I Trauma: An injury (such as a wound) to living tissue caused by an extrinsic agent. 1. SKULL FRACTURES:. important Open vs close fracture X v structure around Skull vault vs skull base (basillar) fracture here Linear vs depressed fracture ear drainage 2. TRAUMATIC PARENCHYMAL BRAIN INJURY CONCUSSION > - bergegar A clinical syndrome of altered consciousness secondary to head injury Due to change in head’s momentum (eg impact with a rigid object) Transient loss of consciousness, respiratory arrest, loss of reflexes Recovery is usually complete Post-concussive neuropsychiatric syndromes may be associated with repetitive injuries Y could get epilepsy attack TRAUMATIC PARENCHYMAL BRAIN INJURY DIRECT PARENCHYMAL INJURY Contusions: bruise caused by blunt trauma Lacerations: injury caused by penetration of object or tearing of tissue Coup injury : Contusion at the point of contact/blow > direct surface E - location Countercoup injury: Contusion at diametrically opposite surface - A. ACUTE CONTUSION - areas of hemorrhage and tissue disruption (arrows) B. OLD CONTUSION - depressed, retracted, yellowish brown patches involving the crests of gyri - A.k.a plaque jaune - reflects hemosiderin accumulation (macrophage eating up old blood) - can become epileptic foci. tearing of brain tissue with breached pia mater  TRAUMATIC PARENCHYMAL BRAIN INJURY DIFFUSE AXONAL INJURY Petechial Haemorrhage Widespread axonal trauma secondary to stretching or tearing of axons. too stretch tear + out Severe rotational/ angular forces Clinical symptoms disproportionately worse than suggested from injuries seen on imaging HPE: axonal swelling (retraction ball) and focal haemorrhages Images from balls - where the axon https://www.ijsr.net/archive/v5i1/NOV153032.pdf  INTRACRANIAL HAEMORRHAGE A * can be cause by non-traumatic Image from: https://www.differencebetween.com/what-is-the-difference-between-intracerebral-hemorrhage-and-subarachnoid-hemorrhage/ TRAUMATIC VASCULAR INJURY : Epidural Haemorrhage Mainly due to trauma Dura is fused to periosteum & supplied by dural arteries Skull fracture / displacement → torn DURAL ARTERY (most common: middle meningeal artery) → extravasion of blood under high arterial pressure dura separated from periosterum → hematoma compresses brain Short lucid period followed by a rapidly evolving neurological symptoms TRAUMATIC VASCULAR freshly clotted INJURY : Subdural blood - below dura - along the brain haemorrhage surface -without extension into the depths of sulci -+ Due to trauma - May cause Tear of the BRIDGING VEIN -> accumulation of blood compression of between the dura and the arachnoid. adjacent brain Risk factors : - Elderly with brain atrophy (stretched bridging veins) : SDH may follow a minor trauma. - Infants (thin-walled veins) Clinical manifestations - Often non-localizing (eg headache and confusion) with slowly progressive neurologic deterioration > clinical - d/t o pressure - finding more general ↓ - May have acute decompensation - Chronic subdural haemorrhage : multiple episodes of repeat bleeding Bridging veins travel from the convexities of the cerebral hemispheres through the subarachnoid space and dura to empty into the dural sinuses. 13 3. SEQUELAE OF CNS TRAUMA CNS has limited capacity for functional repair anatomic location of the trauma determines the consequences of CNS trauma. i.e may be clinically silent (e.g., in the frontal lobe), severely disabling (e.g., in the spinal cord), or fatal (e.g., in the brainstem). neurologic syndromes may become manifest months or years after brain trauma 1) Post-traumatic hydrocephalus due to obstruction of CSF resorption from hemorrhage into the subarachnoid space 2) Chronic traumatic encephalopathy - i.e “dementia pugilistica” : - repeated concussions from head trauma eg professional atheletes - Mood disturbance, behavioral abnormalities, cognitive impairment, motor abnormalities 3) post-traumatic epilepsy 4) risk of infection 5) psychiatric disorders  Young onset Parkinson disease vs repetitive boxing-related head trauma? Okun MS, Mayberg HS, DeLong MR. Muhammad Ali and Young-Onset Idiopathic Parkinson Disease—The Missing Evidence. JAMA Neurol. 2023;80(1):5–6. doi:10.1001/jamaneurol.2022.3584 Non-traumatic brain injury 1) Non traumatic intracranial bleed - Subarachnoid haemorrhage > trauma-caused (common) - - Intraparenchymal haemorrhage (Haemorrhagic stroke) 2) Ischaemic stroke (Focal/ Global) 3)Hypertensive cerebrovascular disease Non-traumatic brain injury 17 Subarachnoid haemorrhage (SAH) Causes of SAH Traumatic Non-traumatic : - ruptured Berry aneurysm - bleeding from tumours - vascular malformation - extension of intraparenchymal haemorrhage  AX BERRY ANEURYSM * Saccular dilatation usually at an arterial branch point along the circle of Willis Risk factors : ▪ Female (1.5x) ▪ Smoking ▪ Hypertension ▪ Most are sporadic ▪ Some genetic eg Marfan syndrome, fibromuscular dysplasia, autosomal dominant polycystic kidney disease Clinical presentation - Sudden excruciating headache with rapid loss of consciousness (“Worst headache of my life!”) - In 1/3 of cases : following increase in intracranial pressure eg straining Junction of the anterior communicating artery with anterior cerebral artery Junction of the posterior communicating artery with the internal carotid artery Bifurcation of the middle cerebral artery Q Saccular dilatation of the vessel i.e thin wall outpouching Site ? - suncion between post communicating a Saccular dilatation Thin wall, dilated lumen Area of rupture Normal arterial wall for Blood clot and haemorrhage comparison  21 Non-traumatic brain injury Intraparenchymal/Intracerebral haemorrhage Rupture of small intraparenchymal vessels present with sudden onset of neurologic symptoms (haemorrhagic stroke) Causes: Hypertension (~50%) Amyloid angiopathy Other vascular causes : vascular malformation, aneurysm, vasculitis Other non-vascular causes: neoplasms, systemic coagulation disorders Hypertensive intraparenchymal haemorrhage 22 /dilatation normal Hyalin deposition in arterioles (hyaline arteriolosclerosis) Charcot-Bouchard microaneurysm  23 ‘Lobar haemorrhage’ - affecting cerebral lobes - Deposition of Aβ amyloid on the wall of medium and small vessels of the meningeal and cortical vessels → weak wall → rupture Amorphous pink deposit within arterioles Positive A-beta stain  Non-traumatic brain injury Cerebrovascular Diseases (CVD) CVD=Stroke Clinical: an episode of acute neurological dysfunction presumed to be caused by ischaemia or non-traumatic haemorrhage, persisting ≥24 hours or until death. The clinical manifestation depends on the site of brain injury, which depends on the vessel involved  Haemorrhagic stroke RUPTURE OF CNS VESSELS : THROMBOLYTIC IS CONTRAINDICATED  Ischaemic stroke Cessation / Impairment of blood suppy and oxygenation A) GLOBAL CEREBRAL ISCHAEMIA B) FOCAL CEREBRAL ISCHAEMIA GENERALISED REDUCTION OF CEREBRAL PERFUSION Cardiac arrest, shock, severe hypotension Area at highest risk : zones bordered by two major arteries → WATERSHED INFACTS Clinical syndrome depends on the severity of insult - Mild : transient confusion and complete recovery - Severe : widespread neuronal injury leading to vegetative state - or death area most common - MCA - ACA  Ischaemic stroke Cessation / Impairment of blood suppy and oxygenation A) GLOBAL B) FOCAL CEREBRAL ISCHAEMIA CEREBRAL ISCHAEMIA CESSATION OF BLOOD FLOW TO LOCALISED AREA OF THE BRAIN - Cerebral infarction is focal brain necrosis due to complete and prolonged ischemia that affects all tissue elements, neurons, glia, and vessels. In situ thrombosis Cause: Atheroma Site: Carotid bifurcation, middle cerebral artery, basilar artery Risk factor: Hypertension, diabetes mellitus, smoking Embolism from distant source Site: Middle cerebral artery and its branch sites Cause : - Cardiac mural thrombus (myocardial infarction, atrial fibrillation, valve disease) - Arterial thrombus (atherosclerosis in carotid artery) Vasculitis Causes: Infection (syphilis, aspergillosis), primary vasculitis.  Ischaemic stroke Cessation / Impairment of blood suppy and oxygenation B) FOCAL CEREBRAL ISCHAEMIA : Infarct types II) Haemorrhagic or red infarct I) Non-haemorrhagic or pale infarct Typically due to emboli - - Typically due to thrombosis - Multiple petechial or confluent haemorrhage - Thrombolytic therapy is beneficial - Due to reperfusion injury - Acute ischemia→ damaged vessels and tissue → reperfusion in the area (due to collaterals and/or dissolution of occlusive material) → blood extravasation  Pathology Changes of Brain Infarct TIME GROSS PATHOLOGY MICROSCOPY Early ( in - basal ganglia C) SLIT HAEMORRHAGE - Hypertension → rupture of small penetrating vessels lake-like B) LACUNAR INFARCT → small haemorrhage → resorbed → leaving slit-like - hypertension → arteriolar sclerosis of deep penetrating arteries supplying basal spaces ganglia, hemispheric white matter, brainstem → occlusion → infarction - Infarcts appear as small, lake-like spaces a.k.a lacunae g O D) HYPERTENSIVE ENCEPHALOPATHY - Acute malignant hypertension → fibrinoid necrosis of vessels → oedematous brain +/- herniation → diffuse cerebral dysfunction - Headache, confusion, convulsion, coma from raised ICP  - dementia * Alzheimer and vascular Dementia loss of f(x) gradually happen together : can  SUMMARY Traumatic head injury is characterized by its relationship with anatomy of scalp, skull, meninges, brain and blood vessels. Intracranial haemorrhage are classified based on its location. It can be traumatic or non-traumatic. Non-traumatic brain injury is frequently vascular related Ischaemic stroke (Focal/ Global) Haemorrhagic stroke Hypertensive cerebrovascular disease  33 REFERENCES 1) Robbins & Cotran Pathologic Basis of Disease 10th edition 2021 2) Anna Hernánde (2021) Basilar Skull Fracture; What Is It, Causes, Symptoms, and More. https://www.osmosis.org/answers/basilar-skull-fracture 3) Mehndiratta P, Manjila S, Ostergard T, Eisele S, Cohen ML, Sila C, Selman WR. Cerebral amyloid angiopathy-associated intracerebral hemorrhage: pathology and management. Neurosurg Focus. 2012 Apr;32(4):E7. doi: 10.3171/2012.1.FOCUS11370. PMID: 22463117. 4) https://radiopaedia.org/articles/subarachnoid-haemorrhage 5) CEREBRAL ISCHEMIA AND STROKE An illustrated interactive course for medical students and residents https://neuropathology-web.org/chapter2/chapter2bCerebralinfarcts.html  34 “I started to feel a bad headache coming on. When I started my workout, my trainer had me get into the plank position, and I immediately felt as though an elastic band were squeezing my brain. The pain—shooting, stabbing, constricting pain—was getting worse. A fog of unconsciousness settled over me’’ SAIt'  35 Michael Schumacher suffered life- changing injuries in a freak skiing accident in 2013. His helmet was cracked in two by the impact. Schumacher initially walked away from the accident after complaining only of feeling a bit shaken. Then he was unable to answer questions coherently and displayed ‘erratic’ behaviour. Schumacher was in a coma when he arrived at the hospital and required immediate surgery on his brain. epidural haemowage O & - O  36 SELF QUIZ Describe the gross finding What is the likely vessel involved Briefly discuss the pathophysiology of this condition  37 SELF QUIZ A 35-year-old woman was brought to the emergency room after a high speed automobile accident. She was found unresponsive at the scene, with little external evidence of trauma. Severe brain injury was suspected. She was pronounced dead upon arrival at the ER. Autopsy revealed petechial hemorrhages within the corpus callosum and superior cerebellar peduncles. What form of injury had most likely be encountered by this patient? Discuss the pathophysiology Describe the likely microscopic finding.  38 SELF QUIZ Describe the gross finding (What? Where?) What is the likely vessel involved? Briefly discuss the pathophysiology of this condition.  39 SELF QUIZ  40 SELF QUIZ  41 SELF QUIZ Describe the gross finding (What? Where?) What is the likely vessel involved? Briefly discuss the pathophysiology of this condition.  42 SELF QUIZ Describe the gross finding (What? Where?) What is the likely vessel involved? Briefly discuss the pathophysiology of this condition.