3/16/99

Pathology II

 

Nervous System

Brain Parenchyma

·        Neurons

·        Framework of glial cells

·        Astrocytes

·        Oligodendrocytes

·        Ependyma—spinal cord tumors

·        Blood vessels

·        Microglial—little macrophages

 

Cells of the Nervous System

·        Astrocytes

·        Major supporting cells

·        Responds to injury by producing dense network of processes

·        Rosenthal fibers—dense aggregates w/in astrocytic cell processes.  Found in slowly growing tumors

·        Alzheimer type II glia—liver failure produces astrocytes w/enlarges, pale nuclei

·        Corpora amylacea—glycoprotein material (amyloid) accumulation in astrocytic processes w/age

·        Oligodendrocytes

·        Wrap around neuronal axons (like Schwann cells)

·        Feature of demyelinating disorders (multiple sclerosis) & leukodystrophies

·        Ependymal Cells

·        Line the cerebral ventricles

·        Ependymal granulations—disruptions due to local astrocyte proliferation

·        Infectious agents may cause ependymal injury, esp. CMV

·        Microglia   

·        Derived from circulating monocytes

·        Major phagocytic cell in CNS

·        Gitter cells—intracellular lipids forming foamy macrophages

 

Edema, Herniation, and Hydrocephalus

·        Fixed boundaries of intracranial vault may result in damage

 

Cerebral Edema

·        Parenchymal edema—2 categories

1. Vasogenic edema—disruption of blood-brain barrier.  Interstitial edema from vascular fluid escapes.  Limited lymphatics impairs brain ability to resorb
2. Cytotoxic edema—intracellular edema secondary to cellular injury, i.e. hypoxic-ischemic insult

·        Morphology

·        Soft tissue "overfills" cranial vault

·        Gyri are flattened—sulci narrowed—ventricles compressed

·        Expansion of brain may cause herniation

·        Herniation

·        3 areas of herniation

1. tonsilar in foramen magnum—cerebral tonsils through foramen

·        life threatening brain stem compression and compromises vital respiratory centers in the medulla oblongata

·        hemorrhagic lesions in midbrain

2. uncinate (transtentorial)—pressure of medial temporal lobe against free margin of tentorium cerebelli

·        3^rd CN compression—pupillary dilation and impaired ocular movement on same side of the lesion

·        Posterior cerebral artery compression—ischemic injury to 1° visual cortex

3. Subfalcine—asymmetrical expansion of cerebral hemisphere displaces cingulate gyrus under falx cerebri

·        Compression of anterior cerebral artery

·        compression of the cranial nerves—look at the dilation of the eye

·        swelling of the brain can cause death

 

Hydrocephalus

·        CSF produced by choroid plexus in lateral and 4^th ventricles

·        CSF circulates through ventricular system, enters cisterna magna at brain stem base via foramina of Luschka and Magendia, then bathes superior cerebral convexities and is absorbed by arachnoid granulations

·        Hydrocephalus—accumulation of CSF in ventricular system.  Usually ¯ resorption is cause

·        Ventricles expand causing ­ intracranial pressure

·        Non-communicating hydrocephalus—when CSF obstruction is w/in ventricles

·        Communicating hydrocephalus—obstruction is outside, i.e. subarachnoid space

·        Before sutures fuse, head will enlarge w/­ circumference

·        After closure, intracranial pressure ­

·        Hydrocephalus ex vacuo—ventricles dilate w/compensatory ­ in CSF as ¯ brain parenchymal

 

Vascular Diseases

·        Normally—brain receives 15% of cardiac output and 20% of oxygen consumed

·        Interruption of blood flow can quickly produce irreversible injury

·        Vascular insults are 3^rd most common cause of death

·        Parenchymal injury—generalized ¯ blood flow—global hypoxia-ischemia encephalopathy

·        Infarcts—local vascular obstruction (80%)

·        Hemorrhages-parenchyma or arachnoid space

 

Infarcts

·        Local circulatory disturbances—80% of CVA

·        Most common in men, in 70's

·        Cerebral atherosclerosis—most common cause

·        Internal carotids

·        Proximal middle cerebral artery

·        Basilar artery

·        Occlusion usually thrombosis over plaque near carotid bifurcation or in basilar artery

·        Other causes :  emboli form heart or proximal carotids—tends to affect

 

Morphology

·        36 to 48 hours—necrotic area becomes swollen and softer

·        1 month—extensive phagocytosis softens, liquefying infarction w/cavitation

·        6 months—completely cavitated

 

Clinical Features

·        infarct typically of sudden onset

·        often preceded by episodes of transient ischemic attacks (TIAs)

·        TIAs—self limiting episodes of vascular obstruction by emboli or platelet-fibrin aggregates

·        1/3^rd of patient w/TIAs develop significant infarct w/in 5 yrs

·        infarcts occur most commonly in areas supplied by branches of the middle cerebral artery

 

Signs and Symptoms

·        contralateral hemipareis and spasticity

·        loss of body sensation on contralateral side

·        visual field abnormalities

·        speech abnormalities when dominant hemisphere is involved

 

·        occlusion of internal carotid artery (thrombosis)—less common

·        infarct of ipsilateral cerebral hemisphere w/monocular blindness (¯ flow ophthalmic artery)

·        arterial anastomoses (Circle of Willis) help supply blood and resulting deficits are lessened

 

Vertebrobasilar system branches also affected by atherosclerosis and thrombosis

·        lesions range from large, rapidly fatal infarcts involving brain stem to small clinically silent infarcts

 

Intracranial hemorrhages

·        1° hemorrhages in epidural or subdural space are due to trauma

·        hemorrhages w/in brain parenchyma and subarachnoid space are due to underlying cerebrovascular disease

 

1° Brain Parenchymal Hemorrhage

·        spontaneous hemorrhage occur mid-to-late adult life, w/peak incidence at age 60

·        most are due to rupture of small intraparenchymal vessel

·        hypertension is most common underlying cause

·        15% of deaths in hypertension patients-1° brain hemorrhage

 

Hypertension and Vascular Effects

·        accelerated atherosclerosis in large arteries

·        Hyaline arteriolosclerosis in small vessels.  These are weaker and more prone to rupture.

·        Charcot-Bouchard micoraneurysms—very small aneurysms associated w/chronic hypertension.  Located in basal ganglion—not congenital; they are developmental(she likes to ask this as a question)

·        Morphology

·        Basal ganglion, esp putamen

·        Thalamus

·        Pons

·        Cerebellum

·        Cerebral white matter

·        Hematomas are well demarcated

·        Large hemorrhages above tentorium cerebelli cause herniation of cerebellar

 

Clinical

·        Abrupt onset

·        Evidence of ­ intracranial pressure

·        Severe headache

·        Vomiting

·        Rapid loss of consciousness

·        Progression of effect noted w/brain stem compression:

·        Deep coma

·        Irregular intermittent respiration (Cheyne-Stokes respiration)

·        Dilated, nonresponsive pupils

·        Spasticity

 

Saccular Aneurysm and Subarachnoid Hemorrhage

·        Most common cause of spontaneous subarachnoid hemorrhage is rupture of saccular (berry) aneurysm

·        1% of general population has berry aneurysm

·        congenital defects in media of arteries at branch points

·        higher incidence in certain disorders:

·        polycystic kidney disease

·        fibromuscular dysplasia

·        coarctation of aorta

·        arteriovenous malformations of the brain

·        80% arise at arterial bifurcation in the territory of the internal carotid artery

·        common sites:

·        middle cerebral artery

·        intracranial branches of internal carotid

·        junction b/w anterior and

 

Morphology

·        wall composed of intima and adventital (no media)

·        compression of adjacent structure "local mass effects"

·        rupture may bleed into subarachnoid space an brain parenchyma

·        infarcts of parenchyma may result due to arterial spasm

 

Clinical Features

·        females slightly more common-usually before age 50

·        abrupt onset w/severe headache, vomiting and loss of consciousness

·        no obvious precipitating factor

·        neck rigidity (meningeal signs)

·        50% die w/in several days

 

Vascular Malformations

·        4 major types

1. Arteriovineous malformations
2. Capillary telangiectasias—small punctuate lesions in pons and cerebral white matter
3. Venous angiomas
4. Cavernous angiomas

 

Central Nervous System Trauma

·        500,00 hospital admissions and 100,000 deaths/yr

·        >70% are permanently disabled

·        most injuries:  blunt trauma (MVA), falls, criminal assaults, including child abuse

·        risk factors:  alcohol abuse, previous head injury, mental retardation, and seizure disorders

·        3 groups of injury:  epidural, subdural hematomas, and parenchymal injuries

 

Epidural Hematoma

·        meningeal artery rupture usually w/skull fracture

·        most common site is branch of middle meningeal artery b/w dura mater and squamous portion of temporal bone

·        fig 23-10

·        Epidural hematomas flatten underlying brain parenchyma.  Rapid expansion due to arterial bleed

·        can produce uncial, gyral, or cerebellar tonsilar herniation; brain stem compression and death

·        many patients have lucid interval immediately after injury, followed by progressive loss of consciousness

 

Subdural Hematoma

·        due to disruption of bridging veins b/w brain surface and draining dural sinuses

·        rapid changes in head velocity:  whiplash injury, blows to head, shaking infant syndrome