Exam 4 - Chapter 28

Question 1

TORCH

Answer 1

TOxoplasma, Rubella, Cytomegalovirus, and Herpes simplex virus 1 & 2
Agroup of infections transmitted from the mother to the fetus with similar clinical manifestations

Question 2

Tay-Sachs Disease

Answer 2

Hexosaminidase A is a lysosomal enzyme that is involved in the breakdown of gangliosides (type of phospholipid), a type of glycolipid found in high concentration in the ganglion cells of the CNS. When this enzyme is deficient, there is the accumulation of GM2 gangliosides, which are toxic to neuronal cells and thus lead to progressive neurologic damage.

Symptoms: Rapid & progressive neurodegeneration, blindness, cherry red macula (eye) & seizures

Question 3

Down’s Syndrome

Answer 3

Causes: Trisomy 21 accounts for 95% of the cases and increase with maternal age
Symptoms: Mental retardation, unique facial features, eye abnormalities, gaping mouth and large tongue, heart diseases, Intestinal defects, Hand abnormalities and Abnormalities of toes.
Diagnostic test: a) Increase in alpha protein, b) Increase of estriol in blood/amniotic fluid of the female

Question 4

Neural Tube Defects (NTD’s)

Answer 4

This group of disorders is characterized by failure of closure of the neural tube. The resulting defects can involve the vertebrae or skull with or without involvement of the underlying meninges, spinal cord, or brain. These disorders are characteristically associated with increased concentration of α-fetoprotein in amniotic fluid or maternal serum. They are also linked with maternal folic acid deficiency

Question 5

Spina Bifida

Answer 5

Failure of posterior vertebral arches to close

• Spina bifida occulta: spina bifida with no clinically apparent abnormalities. It presents as patch of hair overlying the vertebral defect
• Spina bifida cystica: spina bifida complicated by herniation of meninges through a defect. Two types:
a) Meningocele: herniated membranes consisting of meninges only
b) Meningomyelocele: protrusion of meninges and spinal cord

Question 6

Anencephaly

Answer 6

Failure of anterior end neural tube to close. Absence of fetal brain tissue. Usually associated with the absence of overlying skull. Mass of vascular connective tissue mixed with degenerative brain & choroid plexus. Leads to a ‘frog-like’ appearance of the fetus

Question 7

Holoprosencephaly

Answer 7

Failure of embryo’s forebrain to divide into bilateral cerebral hemispheres, leading to incomplete separation of cerebral hemispheres. Leads to facial and neurological defects

Question 8

Encephalocele

Answer 8

Defect in the cranium allows for outpouching of brain through skull

Question 9

Arnold-Chiari Malformation

Answer 9

Small posterior fossa, resulting in downward displacement of the cerebellar tonsils and medulla through the foramen magnum. It often results in pressure atrophy of displaced brain tissue. In addition, it causes hydrocephalus as a result of obstruction of the CSF outflow tract. Associated strongly with thoracolumbar meningomyelocele and stringomyelia

The cerebellar vermis is herniated below the level of the foramen magnum. The downward displacement of the dorsal portion of the cord causes the obex of the fourth ventricle to occupy a position below the foramen magnum. The midbrain shows extreme “beaking” of the tectum with the four colliculi being replaced by a single pyramidal shaped structure

Question 10

Dandy-Walker Malformation

Answer 10

Large posterior fossa with replacement of cerebellar vermis with large cyst; presents as massively dilated 4th ventricle with an absent cerebellum and hydrocephalus. Manifests into seizures and cerebellar dysfunction
Diagnostic tests: a) ultrasound, b) increase in acetylcholine esterase in blood or amniotic fluid.
Prevention: supplement of folic acid ≥ 1000 µg/day to prevent NTDs

Question 11

Hydrocephalus

Answer 11

This condition denotes increased volume of cerebrospinal fluid (CSF) within the cranial cavity and dilation of ventricles. In infants, it is associated with (sometimes marked) enlargement of the skull

Causes: Obstruction to the CSF circulation by congenital malformations, inflammation, and tumors
Pathology: Internal - excessive CSF is present only in ventricular system. External - excessive CSF is present only in subarachnoid space. Communicating - CSF flows freely between ventricles and subarachnoid space. Noncommunicating - CSF flow is obstructed between ventricles and subarachnoid space
Symptoms: Enlargement of the skull in adults, seizures, headaches, visual disturbances, nausea and vomiting ,increased intracranial pressure
Treatment: Ventriculoperitoneal shunt

It can also occur as hydrocephalus without obstruction or increased CSF production in disorders characterized by decreased cerebral mass, such as ischemic brain atrophy or advanced Alzheimer disease

Question 12

Epidural Hematomas

Answer 12

Blood accumulates between dura and skull leading to cerebral compression

Causes: Tearing of middle meningeal artery, middle meningeal vein, or dural sinus, often caused by skull fracture
Pathology: CT scan shows biconcave disk (lens shape lesion) that does not cross suture lines
Symptoms: Loss of consciousness, followed by lucid interval, follwed by headache, followed by rapidly developing signs of cerebral compression. Complications include herniation
Treatment: Surgical drainage of blood, reversal of coagulopathy

Question 13

Bullet Wound Damage to the Brain

Answer 13

The “blast effect” of a high-velocity projectile causes an immediate increase in supratentorial pressure and results in death because of impaction of the cerebellum and medulla into the foramen magnum. A low-velocity projectile increases the pressure at a more gradual rate through hemorrhage and edema.

A bullet that only impacts one hemisphere and misses the central region is less devastating. A bullet that crosses through both hemispheres is usually fatal

Question 14

Subdural Hematomas

Answer 14

Collection of blood between the dura and arachnoid, where blood covers the surface of the brain. Increased rate of occurrence in elderly due to age related atrophy

Causes: Venous bleeding, most often from
bridging veins joining the cerebrum to venous
sinuses within the dura, often caused by head injury
Pathology: Crescent-shaped lesion on CT that crosses suture lines.
Symptoms: Gradual signs of cerebral compression occurring hours to days or even weeks after head injury. Headache, herniation
Treatment: Surgical drainage of blood, reversal of coagulopathy

Question 15

Brain Herniation

Answer 15

Displacement of brain tissue due to mass effect or increased ICP (intracranial pressure)

Tonsillar Herniation: displacement of cerebellar tonsils into the foramen magnum. Compression of the brain stem leads to cardiopulmonary arrest
Transtentorial (Uncal) Herination: involves displacement of temporal lobe. Compression of cranial nerve III: eyes moving down & out with a dilated pupil. The uncus of the para hippocampal gyrus is herniated downward to displace the mid-brain, resulting in distortion of the midbrain with increased anterior to posterior and diminished left to right dimensions. The oculomotor nerve may be compromised, leading to an ipsilateral third nerve palsy

Question 16

Berry Aneurysm

Answer 16

Outpouching of arterial wall, usually at arterial bifurcations of circle of Willis, with intimal thickening and media thinning at neck of aneurysm

Causes: Sproadic, hypertension, cigarette smoking, APKD, connective tissue disorders
Pathology: Media is absent in sac wall. Blood in CSF
Symptoms: Severe headache, nausea and vomiting, fever
Treatment: Surgical repair, coil embolization

Question 17

Subarachnoid Hemorrhage

Answer 17

Bleeding into the subarachnoid space. More frequent in women over 40

Causes: Rupture of berry aneurysm, trauma, arteriovenous malformation
Pathology: CT scan shows blood in basal cisterns, lumber puncture reveals blood in CSF
Symptoms: “Worst headache of my life”, nausea and vomiting, fever
Treatment: High mortality, surgical repair, coil embolization

Question 18

Cushing’s Reflex

Answer 18

Hypothalamic response to ischemia and poor perfusion to the brain

BP: Stroke - decreased. ICP - increased
Pulse: Stroke - increased. ICP - decreased
Respirations: Stroke - increased. ICP - decreased
Consciousness: Stroke - decreased. ICP - decreased

Question 19

Diffuse Axonal Injury (DAI)

Answer 19

A very common result of traumatic brain injury and may result in severe neurological deficits and coma in patients without gross hematomas, contusions or lacerations . However, DAI appears to be a major contributor to morbidity and mortality. There is also increased interest in DAI as a component of military and civilian blast injuries

Question 20

Types of Skull Fractures

Answer 20

Linear/nondisplaced
Depressed
Open
Impaled Object
Basilar (Results in retroauricular ecchymosis (Battle's sign) or periorbital ecchymosis (raccoon eyes))

Question 21

Spinal Cord Injuries

Answer 21

Anterior cord syndrome: Bony fragments put pressure on the anterior portion of the cord resulting in loss of motor movements and pain below the injury
Central cord syndrome: Hyperextension of cervical spine resulting in loss of motor movements in the upper extremity and disruption

Symptoms: Pain, tenderness, deformity (rare), soft-tissue injury, paralysis, painful movement, loss of bowel or bladder control, priapism, impaired breathing

Question 22

Stroke**

Answer 22

Neurologic deficit due to cerebrovascular compromise, major cause of morbidity and mortality
Causes: Ischemia (85% of cases) or hemorrhage (15% of cases). Main factors contributing to stroke: Cerebral thrombosis, cerebral embolus, cerebral hemorrhage and arteriosclerosis of carotid arteries
Hypoglycemic patients mimic stroke symptoms

Symptoms: Facial drooping (usually on one side), headache, aphasia/dysphasia, hemiparesis (weakness on one side), hemiplegia (paralysis on one side), paresthesia (numbness), gait disturbances, incontinence
Diagnosis: It is possible to distinguish a cerebral infarct
from a cerebral hemorrhage by a computed
tomography CT scan. Magnetic resonance imaging (MRI) provides similar information and is equally effective. Manifestations of all these conditions related to strokes, depend on location and size
Treatment: Support ABCs, give oxygen, figure out when the patient was last normal, check glucose, transport to stroke unit. Order CT scan or MRI, obtain 12-lead ECG. Perform neurological exam - if hemorrhage is present, begin stroke pathway. If no hemorrhage, do fibrinolytic therapy if possible and approved, if not, administer aspirin

Question 23

Ischemic Stroke**

Answer 23

80% of stroke cases

Causes: Thrombosis, embolism, dissection, vasculitis, hypotension. Risk factors include hypertension, tobacco use, atrial fibrillation, hyperlipidemia, diabetes
Pathology: Cerebral Infarction - Associated with thrombosis, embolism. Ischemic neuronal change within 12 hours, liquefactive necrosis by 1-3 weeks, gliosis (scar formation) after several months. Watershed Infarction - Associated with hypotension; see wedge-shaped infarction at area supplied by artery, usually between ACA (anterior cerebral artery) and MCA (middle) distribution, Lacunar Infarcts - Associated with hypertension and thrombotic obstruction of small vessels
Symptoms: Depends on site and extent of damage. ACA - Sensory loss and weakness in contralateral leg. MCA - Contralateral paralysis and sensory loss. PCA - Contralateral sensory disturbance
Treatment: Thrombolytic therapy, antiplatelet therapy

Pathogenesis: In a diseased carotid artery (or some other artery if dealing with emboli), the thrombus breaks off and travels to a cerebral artery (ACA, MCA, PCA) in the brain. Thrombus lodges in the artery, restricting blood flow to the brain

Question 24

Hemorrhagic Stroke**

Answer 24

20% of stroke cases

Causes: Hypertension, bleeding disorders, anticoagulant medications, arteriovenous malformations, brain tumors
Pathology: Associated with rupture of Charcot-Bouchard microaneurysms. Hemorrhage usually in basal ganglia or thalamus
Symptoms: Impairment of consciousness, nausea and vomiting, headache, neurological deficits
Treatment: Reverse any coagulopathies, strict BP control, surgical decompression

Question 25

Transient Ischemic Attack***

Answer 25

These brief episodes of impaired neurologic function are caused by a temporary disturbance of cerebral circulation. TIAs are not associated with permanent damage, but are considered precursors to more serious occlusive events. Indicative of carotid artery disease. Symptoms resolve in couple of minutes or hours

Question 26

Pyogenic (Bacterial) Meningitis

Answer 26

Inflammation of the leptomeninges. Meninges
consist of three layers (dura, arachnoid, and pia)
that lie between the brain and the skull. Pia and arachnoid together are known as leptomeninges

Causes: Group B streptococci, E coli, and Listeria monocytogenes (neonates) Neisseria meningitis (children and teenagers), Streptococcus pneumoniae (adults and elderly), and H influenza (non-vaccinated infants)
Pathology: Purulent exudate within meninges, engorged meningeal vessels. Cloudy CSF with neutrophils, increased protein, decreased glucose, increased opening pressure
Symptoms: Altered mental status, photophobia, classic triad of neck stiffness headache and fever. Complications inclde death by herniation secondary to cerebral edema, hydrocephalus, hearing loss, and seizures
Treatment: Antibiotics and steroids

Question 27

Viral Meningitis

Answer 27

Causes: HSV virus, Coxsackievirus (children; fecal-oral transmission), echovirus & fungal (immunocompromised individuals)
Pathology: Lymphocytes with normal CSF glucose. Lymphocytosis, mildly elevated protein
Symptoms: Same as pyogenic
Treatment: Self-limiting, anti-viral drugs, acyclovir

Question 28

Crutzfeld-Jacob (Mad Cow) Disease

Answer 28

Causes: Small prion particle produced and
resistant to heat/sterilization. Only inactivated by 1M
NaOH for 1 hour.
Pathology: The normal form of protein is the “good prion” designated PrPc. The abnormal form of protein is the “bad prion” designated PrPsc. Transmission is thought to be by exposure to (most commonly by ingestion of) prion-containing animal (or human) tissue, particularly, but not exclusively, brain
Symptoms: Spongiform encephalopathy (spongiosis), which is characterized by clusters of small cysts in CNS gray matter, along with a striking absence of inflammatory response
Treatment: Inceration of tainted tissue

Question 29

Guillain-Barré Syndrome

Answer 29

Autoimmune reaction resulting demyelination of peripheral nerves

Causes: Viral (EBV, HSV & CMV) infection causes a T-cell mediated immune reaction
Pathology: Endoneurial and perivenular infiltration by lymphocytes and macrophages. CSF with
large protein count with mild cell count increased
Symptoms: Weakness and tingling in legs and ascending muscle weakness, rapidly progressive paralysis, facial diplegia, abnormal autonomic function. May cause respiratory failure/arrest
Treatment: Supportive/resuscitative interventions and IV IgG. Most recover

Question 30

Multiple Sclerosis

Answer 30

Autoimmune demyelination of the white matter in the CNS

Causes: Idiopathic. Autoimmune, genetic, environmental, distance from equator, HLA-DR2. Mostly affects white women 20-30
Pathology: Demyelination in the white matter of the CNS. Gray-appearing firm plaques in the white matter. Helper CD4+ and cytotoxic CD8+ T lymphocytes and macrophages infiltrate plaques. Depletion of oligodendrocytes, monocytes, lymphocytes, and lipid-laden macrophages around vessels. Gliosis and astrocyte production. Lumbar puncture shows increased lymphocytes, increased immunoglobulins with oligoclonal IgG bands on high resolution electrophoresis and myelin basic protein
Diagnosis: MRI (reveals plaques) and lumbar puncture (reveals IgG bands)
Symptoms: Relapsing neurological deficits with periods of remission. Classic Charcot’s triad of nystagmus, scanning speech, and intention tremor. Motor (muscle weakness, bowel bladder and sexual dysfunction) and sensory (loss of sensitization of touch) impairment of trunk and extremities. Visual impairment (optic neuritis, retrobulbar neuritis, internuclear ophthalmoplegia)
Treatment: Corticosteroids (most common) to reduce inflammation (e.g. oral prednisone and intravenous methylprednisolone and interferons such as Betaseron, Avonex and Rebif). Side effects include liver damage.
Glatiramer (Copaxone). Doctors believe that glatiramer works by blocking your immune system’s attack on myelin. Injected subcutaneously daily. Side effects may include flushing and shortness of breath after injection.
Tysabri (Natalizumab). This drug is designed to work by interfering with the movement of potentially damaging immune cells from your bloodstream to your brain and spinal cord. Tysabri is generally reserved for people who see no results from or can’t tolerate other types of treatments. This is because Tysabri increases the risk of a brain infection (progressive multifocal leukoencephalopathy ) that is usually fatal.
Mitoxantrone (Novantrone). This immunosuppressant drug can be harmful to the heart, so it’s usually used only in people who have advanced multiple sclerosis

Question 31

Lesch-Nyhan Syndrome

Answer 31

Deficiency of HGPRT enzyme (hypoxanthine-guanine phosphoribosyl transferase): self mutilation & involuntary movements

Question 32

Wernicke’s Syndrome

Answer 32

Characteristics include loss of memory & disorientation associated with chronic alcoholism and deficiency of thiamine (vitamin B1). Reversible

Question 33

Koraskoff Syndrome

Answer 33

Characterized by disorientation, insomnia, delusion. Patient often complain of painful extremities with nerve pains. May be irreversible
Delirium: Characterized by rapid onset of disorganized thought process

Question 34

Alzheimer’s Disease

Answer 34

Most important cause of dementia (progressive loss of cognitive functions and a functional decline (loss of memory predominates). Affects 50% of people over 85. Occurs by age 40 in Down Syndrome

Causes: Idiopathic, increased Aβ protein, deficiency of choline acetyltransferase leading to decreased acetylcholine levels. Mutations in Amyloid Precursor Protein (APP), mutations in presenilin genes, and β4, E4 allele of apolipoprotein E
Pathology: Atrophy of the cortical parts of the frontal and temporal parts of the brain, narrowing of the gyri and a widening of the sulci and ventricles. Neuritic plaques (spherical cluster with Aβ amyloid), neurofibrillary tangles (tau protein within cytoplasm which displace nucleus), amyloid angiopathy
Pathogenesis: Aβ amyloid is derived from amyloid precursor protein (APP). APP normally undergoes alpha cleavage (breaks) and beta cleavage results in Aβ amyloid. They then clump together to form neuritic plaques. Amyloid may also deposit around vessels, increasing the risk of hemorrhage. Once plaques form, tau proteins (which stabilize a neurons arms), starts to break down, and also form plaques within the cell. The neuron then shrivels and dies, leaving behind the tangled tau clump (neurofibrillary tangles)
Diagnosis: PET/MRI scan for early diagnosis
Symptoms: Dementia, memory loss, disorientation, aphasias, loss of motor skills, incontinence
Treatment: Acetylcholinesterase inhibitors (Donepezil) or NMDA receptor antagonists (Memantine) to slow progression. Progressive disease with no cure

Question 35

Possible Treatment for Alzheimer’s

Answer 35

Pathological changes in dementia of the Alzheimer’s type and dementia associated with Parkinson’s disease involve cholinergic neuronal pathways that project from the basal forebrain to the cerebral cortex and hippocampus. These pathways are thought to be intricately involved in memory, attention, learning, and other cognitive processes. While the precise mechanism of action for rivastigmine is unknown, it is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by cholinesterase. If this proposed mechanism is correct, the effect of rivastigmine may lessen as the disease process advances and fewer cholinergic neurons remain functionally intact. There is no evidence that rivastigmine alters the course of the underlying dementing process

Question 36

Pick Disease

Answer 36

Cause dementia, affects more women. Causes asymmetrical atrophy of frontal and temporal lobes of brain

Causes: Idiopathic, autosomal dominant mutations on chr 3, 9, and 17
Pathology: Pick cells (characteristically swollen neurons) and Pick bodies (round, silver-staining, neurofilamentous bodies found in cytoplasm of neurons, aggregated from tau proteins)
Symptoms: Dementia, personality changes, abnormal behaviors, speech disturbances
Treatment: Treat the behavioral and language symptoms arise early. Progressive disease with no cure

Question 37

Parkinson’s Disease

Answer 37

Subcortical neurodegenerative disorder. Usually presents in people over 50

Causes: Idiopathic, trauma, dopamine antagonists such as MPTP (methyl-phenyl-tetrahydropyridine), a contaminant in illicit street drugs. Shy-Drager Syndrome (parkinsonism with autonomic dysfunction and orthostatic hypotension)
Pathology: Pale substantia nigra and locus ceruleus, loss of pigmented dopaminergic neurons in substantia nigra with gliosis, Lewy bodies (eosonophilic inclusion bodies in the cytoplasm of neurons). Less dopaminergic neurons leads to loss of stimulation of the basal ganglia motor circuit which leads to bradykinesia. Damaged neuronal pathways from the substantia nigra to the corpus striatum results in dopamine depletion
Symptoms: TRAP (Tremor: pill rolling tremor at rest & disappears with movement. Rigidity: cogwheel rigidity in the extremities. Akinesia/bradykinesia: slowing of voluntary movement & expressionless face. Postural instability). Shuffling gait. 10-15% develop dementia
Treatment: Pharmacologic therapy (L-DOPA, dopamine agonist and deep brain stimulation)

Question 38

Huntington’s Disease

Answer 38

Neurodegenerative disease affecting people ages 30-50, usually resulting in dementia and then death within 10 years

Causes: Autosomal dominant from increased number of CAG repeats on chr 4
Pathology: Atrophy of the cortex and subcortical nuclei, most prominently the caudate and putamen. Degeneration of GABAergic neurons in these areas. Fibrillary gliosis
Symptoms: Chorea (involuntary, gyrating movements), cognitive impairment, mood disturbances, progressive dementia and depression. Suicide is a common cause of death
Treatment: Treating the symptoms. Usually fatal within 10-20 years of diagnosis

Question 39

Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig’s Disease)

Answer 39

Neurodegenerative disease that results in loss of both upper and lower motor neurons. Affects older men and women over 40. It is the most common form of motor neuron disease

Causes: Idiopathic, autosomal dominant with a defect on chr 21
Pathology: Degeneration and atrophy of the lateral corticospinal tracts. Reduced number of anterior horn neurons with reactive gliosis. Neurogenic atrophy with target fibers
Symptoms: Motor weakness and progressive wasting of muscles in the extremities (small hand muscles), spasticity of arms and legs. Atrophy of muscles, fasciculations. Hyperreflexia, positive Babinski sign. Involuntary twitching, slurred speech
Treatment: Supportive care, death from respiratory failure usually within 5 years of diagnosis

Question 40

Neoplasms

Answer 40

Brain tumors have a very high mortality rate
Brain tumors occur at any age
Of tumors, 50% are primary neoplasms
They may be benign or malignant
Malignant tumors of the CNS do not metastasize

Question 41

Astrocytomas

Answer 41

The most common primary brain tumors. Divided based on their infiltration into the surrounding brain parenchyma. Composed of relatively well-differentiated astrocytes

Astrocytomas that do not infiltrate the brain include pilocytic astrocytomas, pleomorphic xanthroastrocytomas, and subependymal giant cell astrocytomas
Astrocytomas that do infiltrate the brain are diffuse astrocytomas, which can be further subdivided
based on grade
A) Low-grade fibrillary astrocytomas are WHO grade II
B) Anaplastic astrocytomas are WHO grade III

Question 42

Glioblastoma Multiforme

Answer 42

Malignant, high-grade tumor of astrocytes. Most common primary malignant CNS tumor in adults. Affects people 40-60 years old

Causes: Idiopathic, genetic mutations in p53 and RB gene
Pathology: Marked anaplasia and pleomorphism, pronounced vascular changes with endothelial hyperplasia occur. Central areas of necrosis and hemorrhage are surrounded by a “pseudopalisade” arrangement of tumor cells. “Butterfly” lesion found in cerebral hemisphere crossing the corpus callosum
Symptoms: Seizures, headaches, nausea and vomiting, other signs of increased ICP
Treatment: Surgery, chemo, radiation. Poor prognosis, death within year of diagnosis

Question 43

Oligodendroglioma

Answer 43

Slow-growing benign tumor derived from oligodendrocytes. Affects middle-aged people and typically arises in the cerebral hemispheres

Causes: Idiopathic, translocation between chromosomes 1p and 19q
Pathology: ‘Fried-egg’ appearance of cells on biopsy. CT scan shows circumscribed, calcified (gray) tumor in white matter (usually frontal lobe) often with cysts, increased vascularity
Symptoms: Seizures, headaches, papilledema, other signs of increased ICP
Treatment: Surgery, chemo, radiation. Average survival time is 5-10 years after diagnosis

Question 44

Ependyomas

Answer 44

This neoplasm most frequently occurs in the fourth ventricle. Peak incidence is in childhood and adolescence

Causes: Arises from ependyma of ventricular system
Pathology: Solid, papillary growths extending from floor of fourth ventricle. Tumor cells often have blepharoplasts (rods near nucleas, which represent basal ciliary bodies). Uniform cells with round nuclei arranged in perivascular pseudorosette formation (encircling vessels or pointing toward a central lumen)
Symptoms: Obstructive hydrocephalus (papillary growths that obstruct flow of CSF through compression of fourth ventricle). Seizures, headaches, nausea and vomiting, other signs of increased ICP
Treatment: Surgical excision (difficult), poor prognosis, average survival time of 4 years

Question 45

Meningioma

Answer 45

Benign, slow-growing tumor arising from the arachnoid meninges (technically external to the brain). Second most common primary intracranial neoplasm (WHO-1 grade). Most common benign CNS tumor in adults. More commonly seen in women older than 30; rare in children

Causes: Idiopathic
Pathology: Presence of psammoma bodies (laminated calcifications) and whorled pattern of ticktly packed tumor cells. Imaging shows round, encapsulated mass attached to the dura. Usually occurs in cerebral hemisphere or parasagittal region. Does not infiltrate the brain
Symptoms: Symptoms associated with compression of underlying brain (see meningitis and such), seizures, headaches, nausea and vomiting, other signs of increased ICP
Treatment: Surgical removal if symptomatic. Good prognosis

Question 46

Schwannoma (Neurilemmoma)

Answer 46

Benign, slowly-growing encapsulated tumor arises from Schwann cells and can affect cranium or spinal nerves.

• When intracranial, it is most frequently localized to the eighth cranial nerve (acoustic neuroma, acoustic schwannoma), which is the third most common primary intracranial neoplasm. It also originates in posterior nerve roots and peripheral nerves.
• It has two patterns:
Antoni A: interlacing bundles of elongated cells with palisading nuclei
Antoni B: looser, less cellular pattern than Antoni A