Gianani CIS Neurovascular Diseases

Question 1

What are the potential neurovascular complications of severe hypertension (with ventricular hypertrophy)?

Answer 1

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

Question 2

aside from HTN, another cause of hemorrhagic stroke

Answer 2

vessel wall fragility

trauma

Question 3

one type of hemorrhage that can be either from trauma OR HTN

Answer 3

subarachnoid

Question 4

name 2 hemorrhages not usually due to HTN

Answer 4

subdural

epidural

Question 5

spontaneous intracranial bleeding causes

Answer 5

coagulopathy

deficiency of platelets*- worry at about 10,000

Question 6

buzzword of “worst headache in life”

Answer 6

often suggests subarachnoid hemorrhage

Question 7

two types of hemorrhage that can be from HTN

Answer 7

subarachnoid

intercerebral

Question 8

CT scan

Answer 8

do it during emergencies

fresh blood and bone are white

Question 9

trouble speaking mean

Answer 9

s probably problems with cortex

Question 10

causes of intercerebral hemorrhage

Answer 10

trauma

subdural, epidural , subarachnoid hemorrhage

Question 11

fibrosis of subarachnoid space –>

Answer 11

hydrocephalus

Question 12

Uncal herniation

Answer 12

from subdural hematoma or other mass effect

–> blown pupil (pushing on CN III)

Question 13

Hemorrhage in the basal ganglia and thalamus with intraventricular rupture

Answer 13

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.

Question 14

Basal ganglia

Answer 14

A region of the base of the brain that consists of three clusters of neurons (caudate nucleus, putamen, and globus pallidus)

Question 15

Duret hemorrhage

Answer 15

pons/ brainstem (in the cerebellum)

Question 16

HYPERTENSIVE INTRACEREBRAL HEMORRHAGE

Answer 16

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.

Question 17

Options for bleeding in hemorrhagic stroke

Answer 17

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.

Question 18

ARTERIAL ANEURYSMS-Rupture

Answer 18

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.

Question 19

Takotsubo cardiomyopathy

Answer 19

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

Question 20

2 things associated with berry aneurysms

Answer 20

coarctation of the aorta

polycystic kidney disease

Question 21

a way to discover if CSF is coming out the nose

Answer 21

transalbumin in the CSF

Question 22

atrial fibrillation –>

Answer 22

turbulent blood flow, clots can get thrown

Question 23

Differential diagnosis of sudden death

Answer 23

Myocardial Infarction.
Pulmonary embolism.
Arrhythmia.
Massive intracerebral hemorrhage.
Acute ischemic stroke impairing autonomic control.

Question 24

our lady with atrial fib and later leukemia– what’s her final pathological dx (sudden death)

Answer 24

Massive basal ganglia hemorrhage secondary to hypertension, thrombocytopenia and anti-coagulant therapy.

Question 25

1) Hypoxic-Ischemic Encephalopathy (HIE)

- Why is the brain so sensitive?

Answer 25

2% of body weight
15% of body energy
15% of cardiac output

Aerobic metabolism
No energy stores
O2 and glucose supplied by circulation

Question 26

HIE starts where?

Answer 26

HIE = hypoxia of the whole brain

HIE is initially a grey matter process and does not affect the white matter

Question 27

A drop in cerebral perfusion, hypoxia, hypoglycemia, extended seizure, or severe anemia can cause –>

Answer 27

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

Question 28

Reperfusion

–>

Answer 28

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.)

Question 29

Global ischemia –>

Answer 29

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)

Question 30

Cerebral infarction =

Answer 30

focal brain necrosis due to complete and prolonged ischemia that focally affects all tissue elements, neurons, glia, and vessels.

Question 31

CLINICAL FINDINGS

in cerebral infarcts

Answer 31

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.

Question 32

Compartments of infarct development

Answer 32

Penumbra: moderate ischemia, delayed infarction

Core: dense ischemia, early infarction

Question 33

cerebral infarct and edema

Answer 33

• 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.

Question 34

basic mechanisms of cell tissue injury in infarcts

Answer 34

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.

Question 35

Bland vs hemorrhagic inarcts

Answer 35

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)

Question 36

Ischemia –> Reperfusion –>

Answer 36

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.

Question 37

causes of cerebral edema in TBI, HIE, brain tumors, meningitis, brain abscess, and other pathologies

Answer 37

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.

Question 38

Transient Ischemic Attacks (TIA)

Answer 38

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

Question 39

ARTERIOVENOUS MALFORMATIONS (AVMs)

Answer 39

• 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.

Question 40

Sturge-Weber Syndrome.

Answer 40

• 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.

Question 41

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.

Answer 41

Cerebral amyloid angiopathy.

Question 42

CEREBRAL AMYLOID ANGIOPATHY

Answer 42

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.

Question 43

Cerebral amyloid angiopathy- summary

Answer 43

• 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.

Question 44

HYPERTENSIVE ENCEPHALOPATHY

Answer 44

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.