Gianani CIS Neurovascular Diseases Flashcards
What are the potential neurovascular complications of severe hypertension (with ventricular hypertrophy)?
Stroke.
a. Ischemic Stroke.- losing blood to an area
b. Hemorrhagic Stroke.- bleeding into the area
Brain is very sensitive lack of oxygen and glucose
stroke = brain infarction –> tissue death, loss of function
aside from HTN, another cause of hemorrhagic stroke
vessel wall fragility
trauma
one type of hemorrhage that can be either from trauma OR HTN
subarachnoid
name 2 hemorrhages not usually due to HTN
subdural
epidural
spontaneous intracranial bleeding causes
coagulopathy
deficiency of platelets*- worry at about 10,000
buzzword of “worst headache in life”
often suggests subarachnoid hemorrhage
two types of hemorrhage that can be from HTN
subarachnoid
intercerebral
CT scan
do it during emergencies
fresh blood and bone are white
trouble speaking mean
s probably problems with cortex
causes of intercerebral hemorrhage
trauma
subdural, epidural , subarachnoid hemorrhage
fibrosis of subarachnoid space –>
hydrocephalus
Uncal herniation
from subdural hematoma or other mass effect
–> blown pupil (pushing on CN III)
Hemorrhage in the basal ganglia and thalamus with intraventricular rupture
This hemorrhage results from rupture of small, penetrating arteries. Hypertensive angiopathy (small vessel disease) stiffens vessel walls and makes them fragile. This, in conjunction with increased pressure from within the lumen, causes vascular rupture and hemorrhage. Hypertensive hemorrhage is parenchymal and its most frequent sites of are the basal ganglia and thalamus.
Basal ganglia
A region of the base of the brain that consists of three clusters of neurons (caudate nucleus, putamen, and globus pallidus)
Duret hemorrhage
pons/ brainstem (in the cerebellum)
HYPERTENSIVE INTRACEREBRAL HEMORRHAGE
15-20% of all strokes…HT, anticoagulants, subarachnoid hemorrhage.
This hemorrhage results from rupture of small, penetrating arteries. Hypertensive angiopathy (small vessel disease) stiffens vessel walls and makes them fragile. This, in conjunction with increased pressure from within the lumen, causes vascular rupture and hemorrhage. Hypertensive hemorrhage is parenchymal and its most frequent sites of are the basal ganglia and thalamus.
Options for bleeding in hemorrhagic stroke
Lenticulostriate arteries
Recurrent artery of huebner
Middle cerebral artery
Frequently it is impossible to know exactly which vessel bled…usually you can determine territory by clinical findings and imaging.
ARTERIAL ANEURYSMS-Rupture
subarachnoid hemorrhage (and high pressure jet bleed into brain tissue)
Intracranial aneurysms (IA), = saccular or berry aneurysms (*Most common cause of fatal non traumatic sub-arachnoid hemorrhage), develop in the walls of major cerebral arteries at branching points, where there are gaps in the media and internal elastica.
The majority of them are on the circle of Willis and the first bifurcation of the middle cerebral artery.
They are multiple in 20% of the cases.
The defects in the vessel wall are present since birth but aneurysms are rare in children; they develop later in adulthood, due to gradual weakening of vessels from the constant force of even normal blood pressure and structural changes that occur with advancing age.
- They are more common in women than men and occur with increased frequency in patients with * coarctation of the aorta and polycystic kidney disease. *
Other risk factors include smoking and alcohol consumption.
Takotsubo cardiomyopathy
also known as transient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, Gebrochenes-Herz-Syndrom, and stress cardiomyopathy is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart.
Because this weakening can be triggered by emotional stress, such as the death of a loved one, a break-up, or constant anxiety, it is also known as broken-heart syndrome.
Stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture
2 things associated with berry aneurysms
coarctation of the aorta
polycystic kidney disease
a way to discover if CSF is coming out the nose
transalbumin in the CSF
atrial fibrillation –>
turbulent blood flow, clots can get thrown
Differential diagnosis of sudden death
Myocardial Infarction. Pulmonary embolism. Arrhythmia. Massive intracerebral hemorrhage. Acute ischemic stroke impairing autonomic control.
our lady with atrial fib and later leukemia– what’s her final pathological dx (sudden death)
Massive basal ganglia hemorrhage secondary to hypertension, thrombocytopenia and anti-coagulant therapy.
1) Hypoxic-Ischemic Encephalopathy (HIE)
- Why is the brain so sensitive?
2% of body weight
15% of body energy
15% of cardiac output
Aerobic metabolism
No energy stores
O2 and glucose supplied by circulation
HIE starts where?
HIE = hypoxia of the whole brain
HIE is initially a grey matter process and does not affect the white matter
A drop in cerebral perfusion, hypoxia, hypoglycemia, extended seizure, or severe anemia can cause –>
a critical shortage of energy (energy crisis)--> energy failure--> depolarization --> loss of function glutamate discharge in synaptic cleft opening of NMDA, AMPA receptors Calcium influx --> activation of catabolic enzymes and activation of NO synthase, NO production --> cellular injury
Reperfusion
–>
Cerebral edema and increased intracranial pressure
1st: intracellular edema
2nd: vascular (endothelial) injury
3rd: interstitial edema
4th: release of intracellular vasoactive metabolites
(arachidonic acid, ect.)
Global ischemia –>
seconds –> electrical activity ceases –> loss of consciousness
Restoration of circulation -> neurons and glial cells return to normal
longer ischemia–> cell membranes compromised, metabolism ceases, neurons die (gray matter more affected)– 4-5 minutes
Irreversible hippocampal, neocortical cell, striatal neurons and Purkinje cell death (> 5 minute)
Cerebral infarction =
focal brain necrosis due to complete and prolonged ischemia that focally affects all tissue elements, neurons, glia, and vessels.
CLINICAL FINDINGS
in cerebral infarcts
Ischemic infarcts cause focal neurological deficits. In embolic infarcts, these appear abruptly. In atherothrombotic infarcts, they evolve over a period of time, usually hours. Atherothombotic infarcts are often preceded by transient ischemic attacks (TIAs). A TIA is a focal neurological deficit that lasts less than 24 hours and resolves. The mechanism of TIAs is uncertain. They may be caused by critical reduction of perfusion that impairs neurological function but falls short of causing permanent tissue damage, or by emboli that break up soon after they occlude vessels.
Compartments of infarct development
Penumbra: moderate ischemia, delayed infarction
Core: dense ischemia, early infarction
cerebral infarct and edema
- release of osmotically active substances (arachidonic acid, electrolytes, lactic acid) from the necrotic brain tissue –> cerebral edema.
- aggravated by vascular injury and leakage of proteins in the interstitial space.
- By 3-4 days, interstitial fluid accumulates in the infarct and around it= most dangerous period for a large cerebral infarct.
- Death from a massive hemispheric infarct is caused by cerebral edema and herniations, not by the loss of brain tissue.
- Recovery of function, after an infarct, is due initially to restoration of perfusion in the penumbra and then to settling down of cerebral edema. Additional improvement may occur later through mechanisms involving neuronal plasticity.
basic mechanisms of cell tissue injury in infarcts
are the same as those with HIE
also: ischemic penumbra: . In every infarct, there is a central core of total ischemia and necrosis which is irreversible. This area is surrounded by a zone of borderline ischemic tissue, the ischemic penumbra. Ischemia, in the penumbra, causes dysfunction due to ionic and metabolic dysfunction but is not severe enough to result in structural damage. Prompt restoration of perfusion in the penumbra by injection of thrombolytic agents may prevent structural damage in this area, thus limiting the neurological deficit. Ischemic stroke is an emergency. The window of opportunity for salvaging the penumbra is very short. If adequate blood supply is not restored within 3 hours, necrosis extends to the penumbra.
Bland vs hemorrhagic inarcts
bland–> swelling and early disintegration of the infarcted area
Hemorrhagic infarct” is usually caused by disintegration of the lesion, caused by an embolus/thrombus, with subsequent reperfusion of blood going into the affected area. (10% of cases)
Ischemia –> Reperfusion –>
Red Neurons
If a patient dies shortly after the insult, the brain is usually grossly and microscopically normal.
If the patient survives and perfusion is restored, changes begin to appear within hours.
causes of cerebral edema in TBI, HIE, brain tumors, meningitis, brain abscess, and other pathologies
accumulation of water in interstitial CNS spaces due to increased vascular permeability (vasogenic edema) and in some cases also by accumulation of water in injured cells (cytotoxic edema). Vasogenic edema involves more severely the white matter and extends along the optic nerves and into the optic papillae (papilledema). The edematous optic papillae protrude forward into the vitreous chamber and displace the retina, causing blurring of vision. Fundoscopic examination reveals blurred disk margins.
Transient Ischemic Attacks (TIA)
Clinical…neurological deficit…typically less than last 10 minutes.
If lasts > 1hr…usually leaves behind small infarct(s).
Important warning sign
Is an emergency…admit, work up
ARTERIOVENOUS MALFORMATIONS (AVMs)
- developmental abnormalities of cerebral vessels.
- tangle of abnormal vessels interposed between a feeding artery and a draining vein.
- Most AVMs are in the distribution of the middle cerebral artery but they may occur anywhere.
- abnormal vessels may be in brain tissue, in the subarachnoid space, or both.
–> seizures and neurologic deficits due to chronic compression and ischemia of brain tissue.
- most feared outcome: intracerebral and subarachnoid hemorrhage.
There may be multiple episodes of bleeding over many years (sometimes since childhood) manifested by headaches, a single catastrophic bleed, or both.
- increased incidence of aneurysms.
Sturge-Weber Syndrome.
- rare, sporadic
- meningeal and ipsilateral cutaneous angiomatosis. –> port wine stain in the face in the distribution of the ophthalmic division of the trigeminal nerve.
- key component of SWS: meningeal angiomatosis.
- pathology in the brain: proliferation of blood vessels in the subarachnoid space, most frequently over the parietal and occipital lobe.
- The underlying brain shows calcified vessels in the cortex and white matter, neuronal loss, gliosis, and laminar cortical necrosis.
- stasis, venous congestion, and ischemia–> progressively damage the underlying brain.
- seizures, developmental delay, transient ischemic attacks, hemiparesis, headaches, and glaucoma.
A 74 year old male experience a spontaneous cerebral hemorrhage. The patient is not on anti-coagulant therapy and does not have hypertension or thrombocytopenia. One of the possible cause of his condition is: A. Sepsis. B. Cerebral amyloid angiopathy. C. Chronic myeloid leukemia. D. Alzheimer dementia. E. Pernicious anemia.
Cerebral amyloid angiopathy.
CEREBRAL AMYLOID ANGIOPATHY
This is not Alzheimer Disease but when AD is present this condition is almost always present !
Most CAA cases are due to deposition of beta amyloid (Aβ), the same peptide that is deposited in the plaques of Alzheimer’s disease (AD). The majority of these are sporadic. The deposition is in small vessels. Deposition congo red +.
The ischemic lesions of CAA cause dementia.
Can cause ischemic or hemorrhagic lesions….vessel lumen can obliterate…vessel wall becomes weak and can break.
Cerebral amyloid angiopathy- summary
- parenchymal brain hemorrhage.
- Insoluble 8-10nm-thick amyloid fibrils are deposited in the walls of leptomeningeal and cortical small arteries, arterioles and capillaries.
- destroys normal vascular elements, makes vessels fragile, causes thickening, and impairs their permeability.
- -> ischemic and hemorrhagic lesions; microinfarcts and a diffuse ischemic degeneration of the white matter (leukoencephalopathy)
- -> leukoaraiosis (literally thinning of the subcortical and periventricular white matter).
- dementia.
- lobar distribution, i.e., they occur in locations other than the thalamus-basal ganglia, which are common sites of hypertensive bleeds.
- CAA-related hemorrhages can occur anywhere; a spontaneous cerebral hemorrhage in an elderly person without an apparent cause should raise suspicion for CAA.
HYPERTENSIVE ENCEPHALOPATHY
Hypertensive encephalopathy (HE) is a syndrome characterized by severe headache, nausea and vomiting, papilledema, visual disturbances, seizures, confusion, and in severe cases coma.
These clinical findings are seen in the background of severe (malignant) hypertension and are accompanied by retinopathy and nephropathy.
In adults, HE is usually the culmination of severe chronic hypertension.
