Stroke Flashcards
1
Q
Define stroke or cerebrovascular accident
A
- acute onset of neurological dysfunction due to abnormality in cerebral circulation
- rapidly developing clinical signs of focal or global disturbance or cerebral function lasting 24hrs or longer
- destruction of surrounding brain tissue
- consequence of changes in both the function of the heart & in the integrity of the vessels providing blood to the brain
-Transient ischemic attack (TIA)/ministroke = when neurological symptoms resolve within 24hrs, a warning sign for a stroke in the near future
2
Q
Vascular requirements of the brain
A
- the brain makes up 2% of the body & receives 20% of the body’s O2 & glucose of cardiac output
- cerebral blood flow (CBF) transports O2 & glucose across the blood brain barrier
- CBF is maintained by a coordinated action of interconnected blood vessels
- CBF if interrupted: brain function stops in seconds while cell damaged occurs in minutes
- CBF is controlled/regulated automatically without being affected much by changes in: arterial pressure, intracranial pressure, arterial blood gases, neural activity, & metabolic demand
3
Q
Death rates from stroke/CVA
A
- 5th leading cause of death & one of the leading causes of disability
4
Q
Incidence rates of stroke/CVA
A
- responsible for 1 in every 20 deaths, every 4 min someone dies from stroke
- someone in the US has a stroke every 40 secs
- 16 million suffer a 1st time stroke each year
5
Q
Non-modifiable risk factors for stroke/CVA
A
- Age: doubles every decade after 55 yrs
- Sex: men > women
- Family Hx: certain genes
- Race: Latin American/African descent
6
Q
Modifiable risk factors for stroke/CVA
A
- Hypertension: >160/95 mm Hg
- Pre-Hypertension: 120-139/80-89
- Cardiac conditions
- Fibrinogen (coagulation factor): increased fibrin deposition
- Diabetes
- Dyslipidemia: low HDL, high LDL
- Sedentary lifestyle
- Obesity: abdominal
- Smoking: increases risk by 50%
7
Q
Types of stroke
A
- Ischemic stroke (87%): thrombotic or embolic occlusion of an artery stopping blood flow to a cerebral area
- Hemorrhagic stroke (13%): bleeding from a blood vessel due to leakage/rupture
- TIA (transient ischemic attack): temporary occlusion of cerebral vessel which gets resolved within 24hrs
8
Q
Early warning signs of a stroke
A
- sudden weakness or numbness of the face, arm, or leg
- sudden dimness or loss of vision, particularly in one eye
- sudden difficulty speaking (slurred) or understanding speech
- sudden severe headache with no known cause
- unexplained dizziness, unsteadiness, or sudden falls
- BE FAST: balance, eyesight, face, arm, speech, time
9
Q
Chances of TIA progressing to stroke
A
- ABCD prediction scale
- age ≥ 60 yrs
- BP ≥140/≥90 mmHg
- unilateral weakness
- speech impairment w/o weakness
- diabetes mellitus
- duration of TIA: ≥ 60 minutes = 2 points; 10-59 minutes = 1 point
10
Q
Pathogenesis of an ischemic stroke
A
- Occlusion of major arteries: thrombus formation narrowing vessel or embolus which has been carried in the bloodstream to lodge in another vessel obstructing blood flow
- Vascular Causes: atherosclerosis or artery to artery embolism
- Cardiogenic Causes: A-fib, MI, or valve disease
11
Q
Cerebral blood flow (CBF) impairments following ischemia
A
- normal CBF = 50 ml/100g/min
- average cerebral perfusion pressure (CPP) = ~60 mmHg
- CBF falls below 20 ml/100mg/min = neuronal functioning impairments
- CBF falls below 8-10 ml/100mg/min = tissue death occurs
- time is tissue: brain ages 3.6 yrs each hour w/o treatment
12
Q
What is the primary goal for treatment of an ischemic stroke
A
- immediate recovery of adequate perfusion in the penumbra to stop progression of infarct zone
13
Q
Events causing secondary neural damage in stroke
A
- mitochondrial energy failure due to lack of O2 in penumbra
- Increased glutamate release -> Ca2+ ions -> excitotoxicity
- Hypoxia-induced free radical production
- Release of degradative enzymes
- Inflammatory responses – leukocytes, cytokines/chemokines
- Activation of glial cells (macrophages, astrocytes) following inflammation
14
Q
Clinical syndrome of ischemic stroke
A
- depends on arterial distribution of the region
- depends on the functional areas affected in the occluded region: need to know the location of the functional areas in the brain
15
Q
Describe the circle of Willis
A
- joins blood supply from 2 arteries to provide collateral circulation to all of brain
16
Q
Describe the middle cerebral artery distribution
A
- biggest distribution
- supplies. the dorsolateral regions of frontal/parietal lobes, temporal lobe, basal ganglia nuclei, & internal capsule
17
Q
Describe the anterior cerebral artery supply distribution
A
- medial regions of frontal & parietal lobes
- anterior region of frontal lobe
18
Q
Describe the posterior cerebral artery supply distribution
A
- occipital lobe
- inferior regions of temporal lobe (hippocampus)
- midbrain (cerebral peduncles)
- thalamus
19
Q
Describe the brainstem & cerebellar artery distributions
A
- collateral circulation provided by a pair of vertebral arteries, to form the basilar artery (vertebrobasilar system supplies brainstem & cerebellum)
20
Q
Describe the SCA supply distribution
A
- SCA (superior cerebellar artery)
- cerebellar cortex
- cerebellar nuclei
- superior cerebellar peduncle
- a small portion of midbrain
21
Q
Describe the AICA supply distribution
A
- AICA (anterior inferior cerebellar artery)
- supplies inferior surface of the cerebellum, cerebellar nuclei, & portions of the pons & medulla
- CN nuclei 5/7/8
- vestibular & hearing organs (helps with differential diagnosis)
22
Q
Describe the PICA supply distribution
A
- PICA (posterior inferior cerebellar artery)
- arises from vertebral arteries
- supplies dorsolateral medulla
- posterior portion of the cerebellar hemispheres
- central nuclei of the cerebellum
- CN nuclei 5/9/10
23
Q
describe the prefrontal area of the cortex
A
- supplied by the ACA (anterior cerebral artery) & MCA (middle cerebral artery)
- behaviors, judgement, foresight, problem solving, social appropriateness
- Lesion = apathy, poor motivation, flat affect, social inappropriateness, perseveration, poor judgement
- due to connections between dorsolateral prefrontal cortex to basal ganglia may have difficulty with dual tasking & motor planning
24
Q
Describe the premotor area of the cortex
A
- supplied by the MCA (middle cerebral artery)
- motor planning area (externally guided movements): reaching, grasping
- Lesion = ideomotor apraxia (inability to perform a task in response to a verbal command or imitate gestures; pt knows what they want to do but cannot plan the muscle coordination needed to complete a task; problems with bimanual tasks
25
Q
Describe the supplementary motor area of the cortex
A
- supplied by the ACA
- motor planning area (internally guided movements)
- Lesion = ideomotor apraxia
26
Q
Describe the primary motor area in the cortex
A
- supplied by the ACA & MCA
- execution of voluntary skilled movements
- Lateral cortex = UE, upper trunk & face
- Medial cortex = LE, lower trunk
- Lesion = lack of voluntary skilled movements
27
Q
Describe the primary sensory area of the cortex
A
- supplied by the ACA & MCA
- detection & localization of sensation from the opposite side of the body & face
- Lateral cortex = UE, upper trunk & face
- Medial cortex = LE, lower trunk
- Lesion = loss of sensation, impaired balance
28
Q
Describe the sensory association area of the cortex
A
- supplied by the ACA & MCA
- sensory processing & sensory perception
- Lesion = ideational apraxia (failure to conceptualize, plan, & execute complex sequences or motor actions involved in using tool bc of loss of perception of the object’s purpose)
29
Q
Describe the frontal eye fields area of the cortex
A
- supplied by the MCA
- controls voluntary saccadic eye movements & smooth pursuits
- Lesion = eyes deviate towards the lesion (look away from paralysis)
30
Q
Describe Wernicke’s area of the cortex
A
- supplied by the MCA & PCA 9dominant hemisphere usually left)
- language comprehension
- Lesion = pt cannot comprehend speech, pt can speak fluently, but output makes no sense, fluent/receptive aphasia
31
Q
Describe the Broca’s area of the cortex
A
- supplied by the MCA (dominant hemisphere usually left)
- expressive language (speak, write, sign, etc.)
- Lesion = inability to express one’s self through language (but comprehension is intact), nonfluent/expressive aphasia
32
Q
Describe the primary visual area of the cortex
A
- supplied by the PCA
- perceives visual info coming from the retina
- Lesion = cortical blindness, loss of vision in contralateral 1/2 of the visual field, but pt may not feel the loss (visual agnosia)
33
Q
Describe the visual associations area & taste/gustatory area of the cortex
A
- Visual association area: supplied by the PCA; makes sense of vision, recognizes faces & objects
- Taste/gustatory area: supplied by the MCA; insular cortex & frontal operculum; detects & discriminates between tastes
34
Q
Describe the internal capsule of the sub-cortical regions
A
- supplied by the MCA (Lenticulostriate arteries)
- Sensory:contralateral loss of pain, temperature, touch and proprioception from entire extremities and face (remember where they relay?)
- Motor: contralateral weakness of all muscles of the body
35
Q
Describe the midbrain of the sub-cortical regions
A
- supplied by the basilar artery, PCA, & SCA
- Sensory: Spinal Lemniscus (Pain and temp), Medial Lemnicus (touch and proprio)
- Motor: Cranial nerve nuclei III, IV, MLF (causes internuclear ophthalmopegia), corticobulbar tract, corticospinal tract
36
Q
Describe the pons of the sub-cortical regions
A
- supplied by the vertebrobasillar system (pontine, AICA, & sub cerebellar)
- Sensory: Spinal Lemniscus (Pain and temp), Medial Lemniscus (touch and proprio), superior olivary nucleus (hearing), main sensory nucleus (sensation from V, VII, IX, X), ½ of the vestibular nucleus
- Motor: Cranial nerve nuclei V, VI, VII, PPRF, corticospinal tract, reticulospinal tract
37
Q
Describe the medulla of the sub-cortical regions
A
- supplied by the PICA & vertebral arteries
Open medulla:
- Sensory: Spinal Lemniscus (Pain and temp), Medial Lemniscus (touch and proprio), cochlear nuclei, spinal trigeminal nucleus (Pain and temperature from V, VII, IX, X)
- Motor: nucleus ambiguous (IX, X), hypoglossal nucleus (XII), lateral vestibulospinal tract, corticospinal tract
Closed medulla:
- Sensory: nucleus cuneatus (touch and proprioception from UE) & nucleus gracilis (touch and proprioception from LE), lateral spinothalamic tract (pain and temp)
- motor: nuclus ambiguous (IX, X), hypoglossal nucleus (XII), lateral vestibulospinal tract, corticospinal tract
38
Q
Clinical manifestations of an MCA syndrome (63% of ischemic strokes)
A
- supplies primary motor & sensory cortices, Broca’s area, & Wernicke’s area
- contralateral weakness (UE & face)
- contralateral sensory impairment (UE & face)
- aphasia (L/dominant hemisphere): expressive, receptive, global
- neglect (R/nondominant hemisphere)
39
Q
Clinical manifestations of an ACA syndrome (6-7% ischemic strokes)
A
- supplies the primary motor & sensory (LE), supplementary motor, & prefrontal cortex
- sensory impairment in contralateral LE
- weakness in contralateral LE
- altered mental status: frontal lobe behavioral abnormalities (poor judgement, decreased attention, decreased motivation, difficulty registering emotions)
- speech perseveration (aphasia)
- abulia (a lack of drive/will power
40
Q
Clinical manifestations of a posterior cerebral artery (12-13% of ischemic strokes)
A
- supplies the occipital lobe, inferior & lateral parts of temporal lobe (hippocampus), diencephalon structures (thalamus & sub thalamus), cerebral peduncles & midbrain
- Contralateral homonymous hemianopsia
- Contralateral limb weakness
- Thalamic pain syndrome (abnormal sensations of temperature/proprioception/touch, tingling, paresthesia, intractable pain, allodynia)
- Disruption of anterior supply – apathy, amnesia
- Disruption of posterior supply – neglect (R hemisphere), aphasia
- Visual agnosia, anomia
41
Q
Clinical manifestations fo a Lacunar syndrome (5-8%)
A
- affects the basal ganglia, internal capsule, thalamus, & brainstem
- small infarcts at the end of deep penetrating arteries, often affecting white matter
- Pure contralateral weakness (posterior limb of internal capsule)
- Pure contralateral sensory loss (posterolateral thalamus or posterior limb of internal capsule)
- Parkinsonism (basal ganglia)
- Large majority are asymptomatic
42
Q
Clinical manifestations of a vertebrobasillar artery syndrome (9%)
A
- supplies corticospinal tracts, corticobulbar tracts, medial & superior cerebellar peduncles, spinothalamic tracts, & several cranial nerve nuclei
-Deficits in sensory and motor cranial nerve functions - Headache, D/N/V, diplopia, nystagmus, dysarthria, dysphagia
- Ipsilateral ataxia (possibly due to double-crossing over of pathways), Hemiparesis, dysmetria
- Bilateral effects if trunk of basilar artery occluded
- Locked in syndrome is due to stroke in basilar artery causing damage to pons/caudal midbrain; total body paralysis, while sparing vertical ocular movement, eye blinking; all sensation is greatly decreased if not absent; cognition and hearing intact
43
Q
Clinical manifestations of a superior cerebellar artery syndrome
A
- supplies the superior cerebellar cortex, superior cerebellar peduncle, cerebellar nuclei, small portions of midbrain/pons
- Headache, D/N/V, Nystagmus, diplopia, dysarthria
- Dysmetria
- Ipsilateral limb/gait ataxia
- Ipsilateral Horner’s syndrome – damage to sympathetic nerves arising from superior cervical ganglion
- Contralateral loss of touch/pain/temp in extremities, torso, and face if any
- Contralateral mild hemiparesis if any
44
Q
Clinical manifestations of an anterior inferior cerebellar artery syndrome
A
- supplies the anterior inferior surface of the cerebellum, cerebellar nuclei, portions of the pons & medulla (CN 5/7/8), vestibular & hearing organs in inner ear
- symptoms referred to as Lateral Pontine Syndrome
- D/N/V, nystagmus, diplopia, dysarthria, dysmetria
- Ipsilateral deafness
- Ipsilateral ataxia, ipsilateral loss of balance
- Ipsilateral Horner’s syndrome (decreased sweating on face, ptosis, constricted pupil)
- Ipsilateral loss of touch/pain/temp and weakness in face
- Contralateral loss of pain/temp and weakness in limbs if any
45
Q
Clinical manifestations of a posterior inferior cerebellar artery syndrome (8%)
A
- supplies the posterior inferior portion of the cerebellar hemispheres, the central nuclei of the cerebellum and dorsolateral medulla (cranial nerve nuclei V/VIII, IX, X)
- Results in Lateral medullary syndrome or Wallenberg Syndrome
- D/N/V, nystagmus, dysarthria (due to both cerebellar and CN IX/X reasons), dysmetria
- Ipsilateral ataxia, ipsilateral loss of balance
- Ipsilateral Horner’s Syndrome
- Dysphagia (CN nuclei IX, X)
- Hoarseness of voice (CN nuclei IX, X)
- Ipsilateral loss of touch/pain/temp on face (CN V nucleus)
- Contralateral loss of pain/temp on body if any
46
Q
Clinical manifestations of a spinal artery & vertebral arteries syndrome
A
- results in medial medullary syndrome
- supplies medial medulla
- paresis of contralateral UE & LE
- contralateral loss of touch & proprioception
- ipsilateral tongue deviation (hypoglossal nucleus)
47
Q
Diagnosis of an ischemic stroke using CT scan
A
- quickly know ‘nature’ of stroke, trade off between increased information about perfusion & the time needed to acquire such information
- CT is the imaging of choice, used due to quickly determine ischemic vs hemorrhagic stroke
48
Q
What is important to know for diagnosing an ischemic stroke
A
- know location & severity of stroke
- quickly know nature of stroke - trade off between increased information about perfusion & the time needed to acquire such info
- CT is imaging of choice to quickly determine ischemic vs hemorrhagic stroke
49
Q
What is the purpose of quick CT for stroke
A
- to make decision about administering r-tPA
- if CT reveals ischemic stroke administer IV tPA within 3 hrs of last known normal and to more selective groups within 4.5 hrs of last known normal
- hemorrhagic stroke would contraindicate use of clot-busting drugs
50
Q
Describe early administration of NIHSS (NIH stroke scale)
A
- not used for diagnosing nature or location of stroke but to assess severity of stroke
- helps with consistent communication
- allows objective measurement of changing clinical status
51
Q
NIHSS scoring
A
- 0 = no stroke
- 0-4 = minor stroke
- 5-15 = moderate stroke
- 16-20 = moderate to severe stroke
- 21-42 = severe stroke
52
Q
Describe diagnosis of stroke using an MRI/PET scan
A
- helps with localizing = lobe, structures that are damaged
- severity/area of damage
- detects the area of ischemic penumbra
- determine who would be a good candidate for continued use of thrombolytic drugs
53
Q
Primary goal of acute care interventions for stroke
A
- reperfusion/recanalization of the occluded vessels using pharmacologic management, end-vascular management, or a combination approach
54
Q
KNOW BP management guidelines (AHA) for acute care interventions for stroke
A
- After rt-PA administration, keep BP less than 180/105
- Not treated with t-PA & plan for mechanical thrombectomy: BP ≤185/110 before procedure and ≤180/105 first 24 hrs after procedure
- Mechanical thrombectomy performed = control BP < 180/105
- Not treated with t-PA or mechanical thrombectomy = permissive HTN up to 220/120, if >220/120 decrease by 15% in first 24hrs post-stroke
55
Q
KNOW Oxygen saturation and surgical intervention guidelines (AHA) for acute intervention for stroke
A
- O2 Sat: maintain ≥94% and supplement O2 if needed to maintain >94%
- Surgical: mechanical endovascular thrombectomy (stent placement) up to 8hrs after Sx onset
56
Q
Blood glucose from new slides***Other acute care pharmacologic interventions for stroke
A
- Once neurologically stable obtain BP 140/90 with use of diuretics & ß–blockers
- Use of anti-thrombotic/thrombolytic agents if indicated but avoid for 24hrs after rt-PA
- Mannitol for edema management as it can increase ICP & put pressure on the cerebellum/brainstem (most common fatal complication)
- Hypoglycemia should be assessed and treated to keep blood glucose between 140-
180 mg/dL as hypoglycemia is related to worse outcome
57
Q
Most common fatal complication of stroke
A
- Edema causing ICP and increased pressure on cerebellum and brainstem
58
Q
Prophylactic interventions for stroke
A
- Anticoagulation
- Lipid-lowering Agents (statins)
- Neuroprotection
- Nerve growth factor
- Surgical intervention
59
Q
Describe anticoagulation as a stroke intervention
A
- Goad standard for prevention of ischemic stroke
- should not be used if at risk of hemorrhagic stroke
- Aspirin, Clopidogrel (Plavix), Warfarinn sodium (Coumadin, Panwarfin), Dabigatran (Pradaxa), Rivaroxaban (Xarelto), Apixaban (Eliquis)
60
Q
Describe neuroprotection as a stroke intervention
A
- compounds that decrease excitotoxicity by reducing glutamate levels
- Magnesium ion, Minocycline
61
Q
Describe nerve growth factor as a stroke intervention
A
- neurotrophic factor that supports the survival & growth of neural cells
- Noggin
62
Q
Describe surgical intervention for stroke
A
- Carotid endarterectomy
- needs to be considered if stenosis is >70% & patient is younger than 80 y/o
63
Q
Describe sub-acute interventions for control of stroke symptoms
A
- Spasticity: Baclofen & benzodiazepines work at the level of the spinal cord; Dantrolene works on the muscle fibers; Botulinum toxin A (Botox) spot specific to muscle injected
- Urinary incontinence: Urge incontinence (anticholinergics); Areflexic bladder (self catheterization or Foley catheter
- Depression: Tricyclic antidepressants, SSRI, SNRI
64
Q
Prognosis based on the NIH stroke scale score
A
- ≥16 suggests a high probability of death or severe debility
- ≤6 suggests good recovery
65
Q
Types of hemorrhagic strokes
A
- Hemorrhagic stroke = bleeding from an arterial source
- Intracerebral hemorrhage
- Subarachnoid Hemorrhage
- Subdural Hemorrhage
- Epidural Hematoma
66
Q
Describe intracerebral hemorrhage stroke
A
- Bleeding into brain parenchyma
- Most deadly subtype of stroke with a 40-50%
mortality - Incidence low among young people, increases
dramatically after 65 years of age - Risk factors – chronic HTN, alcohol abuse,
substance abuse, chronic thrombolytic therapy, smoking, eclampsia during pregnancy
67
Q
Pathogenesis of an intracerebral hemorrhage (ICH) stroke
A
- Dysfunction in cerebral microvasculature secondary to chronic HTN
- Replacement of smooth muscle cells by collagen/fat/amyloid, weakening of arterial walls, formation of aneurysms prone to rupture/leakage,
- Mostly in smaller deep penetrating arteries – lenticulostriates, arteries entering thalamus, brainstem
- Expansion of hematoma – grey matter more prone to compression than white matter
- Blood can be reabsorbed in weeks/months, leaving a cavity surrounded by necrotic tissue
- Damage to brain tissue from lack of blood supply, edema, inflammation, necrosis
68
Q
Clinical manifestations of an ICH (intracerebral hemorrhage) stroke
A
- Similar types of clinical presentation as ischemic stroke
- Initial symptoms are related to area where bleed occurs
- Additional neurologic symptoms occur gradually representing expansion of hematoma
- As bleed enlarges ICP may increase causing headache, vomiting and decreased alertness
- Seizures are possible with cerebral cortex causing the most seizure activity
69
Q
Diagnosis of an ICH (intracerebral hemorrhage) stroke
A
- CT scan: allows prompt diagnosis of ICH; size & location of hematoma; presence & extent of any mass effect
- MRI: limited usefulness in first 24hrs
- Angiograph: performed if patient is young & not hypertensive; cocaine use; to rule out AVM/Aneurysm/Vasculitis or Tumor
- PT/INR & Platelet count: rule out bleeding disorder
70
Q
Treatment for stroke
A
- Needs rapid transport to emergency department due to decreased consciousness & may require intubation
- Decrease elevated BP through use of rapid acting, potent antihypertensive medication; maintain systolic BP <140 (recommend if BP >160-180/105
- Reduce increased ICP using Mannitol in case of cerebral edema
- Anticonvulsants for seizure management
- Emergent surgical draining if neurological condition deteriorates to reduce ICP (especially for cerebellar hemorrhage), may suddenly deteriorate to coma/death
- If on Vit K antagonist (Warfarin), correct INR/PT with Vit K (takes 12-24hrs); fresh frozen plasma (FFP) or prothrombin complex concentrates (PCCs) work immediately
71
Q
Prognosis of a stroke
A
- Mortality is high but functional recovery of survivors is also high if person survives initial changes in ICP
- Size of hemorrhage is greatest predictor of outcome, second is location
- Coma leads to poorer prognosis
72
Q
Describe a subarachnoid hemorrhage
A
- Bleeding into subarachnoid space
- Mostly in older women: >70 y/o
- Risk factors: HTN, alcohol abuse, smoking
- Etiology: Aneuryms and vascular malformations
73
Q
Etiology of subarachnoid hemorrhage (SAH)
A
- Berry aneurysms: abnormal local dissension occurring at vessel bifurcations
- About 90% of SAH are due to berry aneurysms
- Aneurysms are caused by congenital defects & degenerative changes in vessel walls
- Vascular malformations
- Venous malformations
- Arteriovenous malformations (AVMs): direct communication b/w artery to vein; abnormal fetal development
74
Q
Clinical manifestations of SAH (subarachnoid hemorrhage)
A
- Sudden onset with severe thunderclap headache/sentinel headache; sudden intense & persistent, preceding spontaneous subarachnoid hemorrhage (SAH) by days or wks
- Sentinel headache: warning sign of leaks from aneurysm
- At the time of rupture, Sx include nausea/vomiting, altered mental status (syncope, confusion, coma), lethargy, seizure, neck pain, nuchal rigidity
- Focal neurological signs like hemiplegia or hemianopia are absent, unless bleeding into brain parenchyma
75
Q
Medical management of SAH (subarachnoid hemorrhage)
A
- Diagnosis: CT scan, Angio, MRI
- Treatment: Immediate neurosurgery to isolate the aneurysm or rupture site, evacuate hematoma to prevent further damage
- Prognosis: Mortality is high in elderly; If hematoma is <3cm, prognosis is good
76
Q
Describe subdural hemorrhage
A
- Result of tearing of bridging veins b/w brain surface & dural sinuses
- Mostly occur in elderly after falls 2ndy to increased movement of brain inside skulls (due to brain atrophy, fragility of bridging veins)
- If blood accumulates, compression of brain tissue can result in herniation of cortex into adjoining spaces
77
Q
Describe an epidural hemorrhage
A
- Result of tearing of meningeal arteries that run in b/w the dura
- Can be torn 2ndy to trauma
- Medical emergency, need immediate evacuation to prevent compression of brainstem structures, which may cause death
