Flashcards in Module 7 CNS: Stroke, Encephalopathy, Abscess, Meningitis Deck (35):
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
I (intention tremor)
S (Slurred speech)
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?
1. Selective Neuronal Necrosis (unpredictable distribution)
2. Laminar Necrosis: necrosis of all neurons in a given neocortical layer
3. Pseudolaminar Necrosis: necrosis of all cytological elements in neocortical layers 2 thru 6
4. Watershed Infarcts
5. Multifocal grey matter infarcts
What CNS changes are expected in a patient that is dead at a scene?
Massive craniocerebral 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?
Mild diffuse axonal injury
Residual effects of evacuated peridural hematomas
The next topic will be brain abscess, what is the etiology?
Two routes of spread:
1. Hematogenous spread: usually due to sepsis or septic emboli from left sided endocarditis (IV drug users that has tetralogy of fallot)
2. 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)
What is the presentation of a brain abscess?
Projectile vomiting (increased ICP)
Focal neurological deficits
What do you see on biopsy and lumbar puncture in a patient with a brain abscess?
Biopsy best investigation: Mixed flora or Polymicrobal flora (combination of anaerobes and aerobes)
Lumbar Puncture: Elevated WBC, elevated protein and normal glucose (b.c the problem is in the brain not the CSF)
What is seen on CT scan in patient with brain abscess?
CT scan with contrast:
Ring Enhancing lesion
What are the 5 conditions that give you a ring enhancing lesion on CT?
What are the complications of a brain abscess?
Rupture into ventricles ----- ventriculitis ---- obstruction of ventricles ---- hydrocephalus (non communicating)
Also from broad spectrum abx = CDIFF or toxic megacolon
A quick review on Meningitis, what are the bacterial causes for the various age groups?
-Neonate: E.coli or strep
---Children: H.influenza or N.meningitides
-Adolescents: N. meningitides
-Adults: S. pneumoniae or L. monocytogenes
What is seen on histology and CSF for meningitis?
Histology: Exudates covering the leptomeninges and engorgement of the meningeal vessels
CSF: increased WBCs, increased protein and decreased glucose
Fungal Meningitis usually occurs in the immunocompromised, what are the various bugs?
-cryptococcosis: soap bubble appearance
Vasoinvasive --- thrombotic occlusion--infarction and hemorrhage
The last meningitis to be discussed is Tuberculous meningitis. What are some features?
--TB granulomas in the parenchyma (TB)
--May complicate primary hematogenous dissemination
--Cell mediate immunity -- formation of Rich's/Gohn's Focus -- depression of CMI --- reactivation and rupture of focus into subarachnoid space
Moving on to viral encephalitis, what is this?
Perivascular lymphocytic infiltrate
Individual neuronal necrosis with phagocytosis
Focal collection of microglia
Now there are various viral infections that cause encephalitis, each card will go through the various causes, what is the most common viral cause?
HIV-E = most common world wide
The next viral encephalitis is Herpes virus, explain the various herpes viruses that cause encephalitis
Agressive encephalitis in immunocompromised hosts
-Herpes Simplex (HSV 1 &2)- acute necrotizing encephalitis
*edema, focal hemorrhagic necrosis, asymmetric involvement of temporal lobe
*Burn Out HSV: extensive cavitation & gliosis
*Neonatal HSV: 1=postnatally and 2=delivery
-VZV infection: cerebellitis, meningoencephalitis, encephalitis, and myeloradiculitis (also caused by CMV & HSV2)
-EBV: aspetic meningitis
The next viral encephalitis is Rabies (Rhabdovirus-RNA), explain the complications of rabies encephalitis?
Transmitted by bite of rapid animal
--replicates in muscle -- retrograde axonal transport to CNS
--anterograde axonal transport to salivary and lacrimal glands
--Incubation period shorter in children and with bites closer to CNS
-Lymphocytic meningoencephalitis, neuronophagia, extensive neuronal invasion (Negri Bodies =cytoplasmic inclusions)
The next viral encephalitis is HIV, what are some complications of this?
HIV: infects microglial cells and macrophages -- patchy loss of myelin
--widespread mild inflammation: perivascular lymphocytosis, microglial nodules and multinucleated cells
The final viral cause of viral encephalitis is JC virus, w hat are some complications?
JC virus: reactivation of polyomavirus-- progressive multifocal leukoencephalopathy in immunosuppressed patients
--enlarged virus laden oligodendrocytic nuclei and multiple foci of demyelination
Briefly, lets touch on parasite infections of the brain. The first is Toxoplasmosis Gondii, what are some features?
Definitive Host= Cats
Acquired by consumption of undercooked meat or ingestion of contaminated cat feces
Usually immunocompromised patients
Ill-defined multiloculated and necrotizing abscess in deep grey matter (MULTIPLE RING ENHANCING LESIONS)
Finally the other parasitic infection of the brain is Cysticercus Cellulose, what are some features?
Larval form of pork tapeworm = Taenia Solium
Definitive host = humans
Cysticercosis occurs when humans become the intermediate host
Involvement of subarachnoid space -- racemose cysticercosis
Finally the last topic for this card deck is prion disease, what is the cause?
CJD: sporadic -- rapidly progressive dementia and myoclonus
Variant CJD: associated with BSE meat consumption (slower onset and more personality changes)
What is the pathogenesis for prion disease?
Accumulation of altered form of prion protein --- neuronal death, gliosis, accumulation of extracellular amyloid (Kuru plaques) and vacuolization of grey matter
(natural prion protein converted to neurotoxic prion protein)