Module 7 CNS: Stroke, Encephalopathy, Abscess, Meningitis Flashcards
Next topic for CNS is Ischemic Stroke/Cerebral Infarction. there are three types each card will go through the types. What is the first?
Thrombotic/Ischemic Stroke (more common)
HTN — atherosclerosis — unstable plaque —thrombosis —bland infarct (white infarct due to 100% occlusion of lumen)
Risk factors for atherosclerosis:
-smoking, DM, hypercholesterolemia (most common under 40) , HTN (most common over 40)
The second etiology for an ischemic stroke is embolic stroke. What are some features?
Embolic Stroke: (less common but more serious)
–atrial fibrillation + mural thrombus in left heart — legs (DVT) or brain (Red infarct bc lumen not completely occluded)
The third etiology for an ischemic stroke is carotid artery dissection. What are some features?
Carotid Artery Dissection: young and middle aged
- mild trauma — occludes lumen and causes stroke
- -extension to the adventitia may cause subarachnoid hemorrhage
What is the most common affected vessel?
Middle cerebral artery
–watershed between MCA and ACA
What is the presentation of a patient with an Ischemic stroke?
Contralateral hemiparesis and sensory loss (again for any stroke) Aphasia if Broca's Affected Cerebellum affected: D (dysmetria) D (Dysdiadokinesia) A (ataxia) N (nystagmus) I (intention tremor) S (Slurred speech) H (hypotonia)
In an ischemic stroke what does the CT show?
Non contrast CT: shows no abnormalities so that rules out hemorrhage but does not rule out ischemic
MRI: much more sensitive
What changes are seen in the brain for an ischemic stroke?
0-12 hrs: nothing
12-24 hrs: coagulative necrosis
24 hours: PMNs
–stroke is a permanent neurological deficit after 24 hours (legs recover before arms)
–before 24 hours (transient ischemic attack but can still have perm neuro damages)
over 48 hours: microglia – liquefactive necrosis
2 weeks: astrocytes — glosis
Moving on to Hypoxic-Ischemic Encephalopathy, what is this?
Widespread injury to neurons
- -neurons are more vulnerable to hypoxia/ischemia than other cells (4 minute rule on CPR)
- -usually due to cardiorespiratory arrest with resuscitation
What are the pathological changes in order of severity for Hypoxic-Ischemic Encephalopathy?
- Selective Neuronal Necrosis (unpredictable distribution)
- Laminar Necrosis: necrosis of all neurons in a given neocortical layer
- Pseudolaminar Necrosis: necrosis of all cytological elements in neocortical layers 2 thru 6
- Watershed Infarcts
- Multifocal grey matter infarcts
What CNS changes are expected in a patient that is dead at a scene?
Massive craniocerebral trauma
Vertebrospinal trauma
Diffuse post traumatic vascular injury
Idiopathic cardiorespiratory dysfunction following milder head injury
What CNS changes are expected in a patient that is in a persistent coma/vegetative state (often with disproportionately mild imaging findings)
Diffuse axonal injury
Post traumatic hypoxic-ischemic encephalopathy (thalamic involvement)
What CNS changes are expected in a patient with a lucid interval (patients who talk and die)?
Acute peridural hemorrhage (epidural hemorrhage)
Post traumatic brain swelling
What CNS changes are expected in a patient with a post traumatic epilepsy, cognitive and/or motor dysfunction?
Contusion
Mild diffuse axonal injury
Chronic Subdural
Residual effects of evacuated peridural hematomas
The next topic will be brain abscess, what is the etiology?
Two routes of spread:
- Hematogenous spread: usually due to sepsis or septic emboli from left sided endocarditis (IV drug users that has tetralogy of fallot)
- Direct/Contigual Spread (more common): sinusitis, mastoiditis, otitis media and dental infections
- -example: Chrug Strauss – CANCA positive with chronic sinusitis
What is the pathogenesis for a brain abscess?
Collection of infection in the parenchyma (liquefactive necrosis with PMNs and cellular debris)