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525 patho exam 2


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How do we know that neurons are metabolically active cells?
large nucleus
many organelles
a lot of mitochondria
produce alot of ATP
require an abundant supply of O2
(lack of O2 for more than 4 minutes = cell death)
What is the carcinogenic potential for neurons?
Low - because they are postmitotic
Characteristics of spinal motor neurons.
Extend out away from spinal cord, cell body in ventral horn, super long.
Characteristics of spinal sensory neurons.
Dorsal root ganglion receives input.
Characteristics of cranial nerves.
Motor neurons serving the head and neck, interface with the medulla or brain stem.
Where are upper motor neurons found?
cerebral cortex
What is a ganglia?
collection of cell bodies of upper motor neurons in the cerebral cortex.
bring input into cell body
take information away from cell body
connection between 2 neurons
How is communication mediated between neurons at a synapse?
chemically - with a neurotransmitter
substance that is released by a presynaptic neuron (in response to an AP in that neuron) that diffuses across the gap to the postsynaptic neuron, binds to a receptor and elicits a response in the postsynaptic neuron.
Common examples of neurotransmitters
acetylcholine, norepinephrine and dopamine are most common examples of neurotransmitters
The connection between neurons may be ---------- or --------- depending on the events that occur in the postsynaptic cell in response to the neurotransmitter
The connection between neurons may be excitatory or inhibitory depending on the events that occur in the postsynaptic cell in response to the neurotransmitter
What is the aim of modern neuropharmacology?
Modern neuropharmacology is aimed at maintaining or restoring normal neurotransmitter balance within neurons of the brain.
The support cells of the CNS:
Glia (neuroglia):
3.Microglia – not discussed
All of the support cells in the CNS are...
facultatuve mitotic cells
Large star shaped cells, cytoplasmic processes link neurons and blood vessels
1.function in metabolism of neurotransmitters to form the blood brain barrier (BBB)
3.function to maintain extracellular fluid balance
*network of support for neurons because no lymphatic system in brain
Cytoplasmic processes of myelinated nerve fibers. myelin- insulation – make transmitting AP faster
In peripheral nervous system, Schwann cells are equivalent
Myelin allows for very rapid conduction of AP’s
=Provide support
-regulate extracellular fluid like astrocytes
-most common glial cell (essentially a lipid layer coating the axon)
gray – unmyelinated, neural cell bodies
white – myelinated, cellular processes (no cell bodies)

Myelin serves to insulate the neuron and allows for increased speed of the AP propagation

*Some disease states affect the myelin sheath - MS
What cells line the ventricles and central canal of the spinal cord and have cilia to promote flow of CSF?
Ependymal Cells
what makes up the Central Nervous System?
brain and spinal cord
What makes up the Peripheral Nervous System?
Peripheral sympathetic and parasympathetic nerves and the autonomic ganglia.
What are the 3 distinct brain regions?
Hindbrain (most primitive, 1st to develop) - medulla, pons, cerebellum
Forebrain - cerebrum, thalamus, basal ganglia, hypothalamus
What functions is the frontal lobe associated with?
motor, problem, solving, spontaneity, memory, language, initiation, judgment, impulse control, social and sexual behavior
Functional regions of the parietal lobe.
1.sensation and perception
2.integrating sensory input, primarily with the visual system
Function of occipital lobe.
vision and the interpretation of vision
Function of temporal love.
auditory sensation, language, and perception
Function of basal ganglia.
integration centers for sensory information ascending to the cortex and motor information descending to lower levels;
monitors what SHOULD BE occuring with WHAT IS occuring;
Coordinating muscle movement (fine adjustments)
Function of amygdala.
center for emotions (fear, confusion, distrb. awareness, amnesia, rage)
Function of hippocampus.
short term memory, spatial orienting/processing info as it enters the brain;
largest neurons-prone to ischemic attack (result: s-t memory loss)
Function of thalamus.
integrating sensory stimuli;
acquisiton of knowledge and awareness
Function of hypothalamus.
integration of temp., HR, BP, thirst, appetite;
releases neurosecretory substances which activate pituitary (via neurons) to release hormones
Function of hindbrain.
1st part to evolve;
reflex circuit
low-level processing;
pons, medulla oblongata, cerebellum
Function of pons, medulla oblongata.
-most primitive
-visual/auditory reflex ctrs.
-cardiac centers
-rate/force of contraction
-vasomotor center-BV tone
-respiratory ctrs. - rate
-origin of most cranial nerves
Function of the cerebellum.
major integrator of motor function
-damage to the cerebellum affects coordination of limb and eye movement
-compares what should be occurring with what is actually occurring - sends error messages to other areas
-determine our position in time and space
-damage results in ataxia, dysmetria, diffulting moving quickly, delayed initiation/termination
postural instability
disturbance of the trajectory or placement of a body part during movement
Function of the midbrain (mesencephalon).
all ascending and descending information to or from the cerebral cortex must pass through
Function of the peripheral nervous system.
nerves from CNS and the autonomic nervous system, including cranial nerves
Function of the spinal cord.
outer white matter and inner gray (opposite of brain tissue)
gray - neuron cell bodies
white - myelinated fibers and unmyelinated from ascending sensory or descending motor neurons

-motor root - going out
-sensory root - coming in
dorsal root ganglion - cell bodies for all sensory nerves
Function of Meninges.
protective covering of brain and spinal cord.
Pia (innermost)
-brain injury will result in bleeding in at least one of the layers
Function of Cerbrospinal Fluid (CSF).
Produced in choroid plexus (a series of specialized capillaries, it flows throughout the ventricular system and exits through lateral openings or a medial opening into the subarachnoid space (bathes brain, cushions brain).
-Can also enter the central canal of the spinal cord.
-Low pressure
-fast turnover (3x a day)
-distinct composition and pressure - alterations in ions, cells, pressure indicate disease
An increase in CSF pressure is caused by ...
-increased polymorphonuclear leukocytes - bacterial infection (and acute inflammation)
-increased lymphocytes - viral infection (meningitis)
-decreased glucose concentration - bacterial infection (meningitis) – bac. use glucose for food
Function of Blood Brain Barrier
-capillary endothelial cells and glial (astrocyte) cellular processes make a thick basement membrane
-glucose, alcohol, amino acids, oxygen and carbon dioxide readily penetrate
-diffusion of lipids limited by size - one reason the brain can not metabolize fat to produce ATP – only glucose!
-only certain antibiotics gain access to brain: erythromycin and sulfadiazine
-insulin cannot cross
How is blood supplied to the brain?
internal carotid --> circle of Willis on base of brain (circles the stalk of pituitary)
vertebral arteries, R & L vertebrals merge to form basilar; serve the pons, medulla, cerebellum
3 major branches from the circle of Willis:
1.Anterior cerebral - supplies structures on the front of the brain
2.Posterior cerebral - supplies the back of the brain
3.Middle cerebral - supplies almost all of the lateral aspects of the brain – the largest portion
Inability to comprehend and integrate receptive language or use language or both.
-∑ associated with lesions to the dominant cerebral hemisphere
-extent of the lesion(s) determine(s) the extent of damage
Wernicke’s Aphasia
damage to area where understanding and interpretation of word symbols occurs (in the dominant hemisphere);
lesions result in impairment in comprehension of speech
-patient is unaware of a problem
-affected persons have fluent, spontaneous speech with normal rhythm and articulation - word salad
-comprehension, repetition and naming are impaired
Broca’s Aphasia
Lesion located in frontal lobe just in front of motor area
-individual may not be able to utter a word or have limited speech
-fully comprehends spoken word
-fully aware - FRUSTRATION
Global Aphasia
-large lesions to both Broca and Wernicke’s area in dominant hemisphere
-all aspects of speech involved
-patients usually have hemiplegia and are unable to comprehend or speak
Which hemisphere is dominant in most people?
>90% of right handed people are left hemisphere dominant
loss of function and this includes both spastic and flaccid paralysis;
usually defined in terms of injury to upper motor neurons and lower motor neurons
-Upper at higher levels of the brain and spinal cord
-Lower at the level of the spinal cord OR peripheral nerves
2 types of paralysis
1.Spastic paralysis – muscles are hard, rigid and difficult to move a joint; can exhibit hyperactive reflex activity
2. Flaccid paralysis – muscles flaccid with lack of reflex activity
Characteristics of Upper Motor Neuron Injury
Spastic paralysis, hyperreflexia, Babinski sign, muscle atrophy (develops over a few weeks)
Characteristics of LMN injury.
Flaccid paralysis - loss of muscle tone
loss of peripheral reflexes occurs
-no Babinski
-significant and prompt muscle atrophy
What is the most common CNS malformation?
Neural tube defects - failure of the neural tube to fuse.
-spina bifida
When does closure of the neural tube start and finish?
start: 22nd day, finishes: 28th day of gestation
This is a catastrophic defect resulting in failure of the brain to develop.
Anencephaly - cerebrum does not develop, most common neural tube defect (1/500 preg.) May be carried to term but infant dies soon after. Higher in women over 40 (Ireland sees it in 1/200.) preg.)
A group of neural tube defects in which the area affected is in the lower back.
Spina Bifida - 4 kinds
Occulta (mildest; hair)
Rachischisis (most severe)
What is Spina Bifida Occulta?
This defect is a lack of development of vertebral arches. Skin usually covers the defect- hair usually seen over the defect. Neural elements are in the normal location.
What is Meningocele?
Protrusion of meninges (ballooning) through a defect in the spinal column. Neural elements in normal location.
What is Myelomeningocele?
Protrusion of meninges (ballooning) through a defect in the spinal column with protrusion of cord elements.
What is Rachischisis?
Most severe form neural tube fails to close and open to the elements, brain is open to infection.
What nutrient reduces incidence of neural tube defects?
folic acid - essential for formation of nucelotide base thymine.
What should women of reproductive age who are sexually active should take a supplement of folic acid?
Because whether they intend to become pregnant, if they do, defects would occur prior to time woman knows she is pregnant.
What are the types of traumatic head injury?
What is a concussion?
Blunt head trauma characterized by loss of consciousness; no significant macroscopic or microscopic changes to the brain.
What is a contusion?
Disruption of cerebral and/or meningeal blood vessels by severe blunt trauma; associated with considerable mortality.
What is a laceration?
Open trauma to the brain tissue; highly fatal.
What is cerebral edema?
Fluid accumulation within the brain;
two types: cytotoxic and vasogenic - closely related.
What is cytotoxic edema?
Cellular dysfunction or injury due to loss of cellular ability to regulate water.
Anything that causes loss of ATP to power the pumps will result in cytotoxic edema. If Na/K pump fails then Na accumulates --> water follows.
*Intracellular accumulation
What can cause the loss of ATP to run Na/K pumps?
metabolic disorders
What is vasogenic edema?
Edema characterized by increased vascular permeability from damage to or dysfunction of cerebral vessels.
-composition of the fluid is similar to plasma – plasma proteins and it accumulates in the interstitial space.
-this protein draws fluid by osmotic forces
-lack of blood flow results in cytotoxic edema
Vasogenic edema results in...
cytoxic edema.
What are the clinical signs of cerebral edema?
increased intracranial pressure --> decreased cerebral blood flow --> decrease in cerebral function --> hernaitions of the brain (through foramen magnum)
-brain appears heavy; wet
-sulci are obliterated, ventricles flattened, subarachnoid space lost.
This is frequently seen in shaken baby syndrome or following major trauma to the brain.
Cerebral edema
This is a lay term for the slow or sudden onset of a series of neurological symptoms; a disease of old age and related to atherosclerosis of cerebral arteries.
What causes stroke?
1.Occlusion of cerebral vessels - from atherosclerotic narrowing of an artery, thrombus formation or lodgement of an embolism, or by
2.hemorrhage - from intracerebral, subarachnoid or AVM (arteriovenous malformations) bleeding.
What are factors that favor the development of stroke?
hypertension, diabetes and thromboembolism
What is the result of stroke?
ischemia and necrosis to the brain
What is a TIA?
Transient Ischemic Attack - lasts for a few minutes to a few hours and the neurological deficits resolve.
-first sign of atherosclerotic narrowing or cerebral vasoconstriction
What is occlusive cerebrovascular disease?
Includes atherosclerosis, cerebral thrombosis (usually of an atherosclerotic plaque) and cerebral embolism
-these have a final common pathway, even though pathogenesis of each is different.
What is cerebral atherosclerosis?
cerebral arteries undergo the process of atherosclerosis -->
formation of an atheroma that projects into the vessel lumen --> inhibits blood flow --> ischemia
-primary cause of TIAs
-if lesion ruptures --> thrombus forms --> aggravates vessel narrowing
What is the leading cause of CVAs?
Cerebral Thrombosis
Where do cerebral thromboses usually cause an occlusion?
curves and bifurcations of vessels - why? turbulence --> endothelial injury
How quickly can cerebral thrombosis occur?
gradual: thrombus forms on existing plaque over time causing occlusion
rapid: ischemic infarction from an embolus dislodged from an atherosclerotic plaque that moves to the brain.
What is the usual cause of death with cerebral thrombosis?
cerebral edema (3-5 days later) from both cytotoxic and vasogenic mechanisms
The clinical presentation of cerebral thrombosis.
gradual or more rapid occlusion of middle cerebral artery (#1 cause) results in contralateral hemiplegia,
sensory loss, bilateral symmetrical loss of vision in half of the visual field, headache, vertigo, confusion, aphasia, other focal neurological signs
-global aphasia can occur if dominant hemisphere affected
Characteristics of cerebral embolism.
-source from heart due to atrial fibrillation, bacterial endocarditis, valvular disease
-also from dislodged thrombus on atherosclerotic lesion
-can cause massive infarction
What is hemorrhagic cerebrovascular disease?
intracranial bleeding.
ex: intracerebral hemorrhage, aneurysms
What is an intracranial hemorrhage?
rupture of blood vessel due to congenital abnormality (aneurysm); rupture caused be traume or through other mechanism like HTN.
-4 groups based on location
epidural, subdural, subarachnoid, intracerebral
What is an epidural hematoma?
Hematoma located between the skull and dura usually due to tear in a meningial ARTERY.
-causes pressure on brain, coma, and death
Tx - drill hole in skull to drain blood
What is a subdural hematoma?
Hematoma located between the dura and the arachnoid layer, usually due to rupture of thin walled bridging VEINS that traverse this area.
What is a subarachnoid hemorrhage?
Ruptured cerebral vessels due to: arteriovenous malformations or rupture of berry aneurysms caused by trauma to cerebral vessels on the surface of the brain.
-BLOOD IN CSF (arterial bleed in subarachnoid space)
What is an intracerebral hemorrhage?
bleeding within the brain; results from rupture of small vessels damaged by HTN. Common site is basal ganglia.
Presents like cerebral embolism but more dramatic and severe headache.
Berry Aneurysm - subtype of hemorrhage in the subarachnoid space. A defect of weakness of cerebral arteries --> outpouching. Originate in circle of Willis --> can be silent then rupture with HTN.
S&S: blood in CSF, very different treatment if hemorrhagic (vs. occlusive)
Neoplasms of the CNS
These are relatively rare, and can occur at any age but more prominient in youth and elderly.
50% tumors are primary
50% are metastatic
Why are malignant neoplasms of the CNS hard to treat?
Difficult to differentiate normal brain from the highly infiltrative malignant tumor.
Why do primary malignant tumors not metastatize?
Because of the BBB, no lymphatics in the brain.
Clinical manifestations of intracranial tumors:
highly variable
headache, vomiting, papilledema (eyes - fundus bulging)
paralysis, seizures, memory loss, visual field defects, cranial nerve dysfunction, mental status, speech disorders, tongue dev. to one side
Classification of CNS tumors
tumors of glial cells (75%)
tumors of the meninges (15%)
Other 10%
a type of astrocytic glioma; occure as
1.solid cerebral tumors in adults
2.cycstic cerebellar tumors in children
-slow growing, well-differentiated astrocytes
Glioblastoma multiforme
-Most common CNS malignancy
-more malignant than astrocytomas
-peak incidence at age 65
-irregular shape, pooly demarcated from normal brain parenchyma
-highly infiltrative and vascular tumor, very rapid growth, no resemblance to parent cell
-in cerebral hemispheres - usually frontal lobe, in middle-age adults
-lesions well circumscribed, cystic, calcified (dystrophic)
-well-differentiated cells
tumors derived from ependymal cells
-malignant and benign
-ventricular ependymomas in children
-spinal ependymomas in young adults
S&S: muslce weakness, disuse atrophy, sensory loss
Prognosis of gliomas
gliobastoma multiforme - fatal
astrocytomas - 5 yrs (poor)
cerebral oligodendrogliomas & ependymomas - better, but needs early detection
tumor of the meninges
-benign lesion - in women after 70
-S&S: seizures, headache, visual impariment, hemiparesis, aphasia, compression of brain
-can be surgically removed; excellent prognosis
metastatic tumors
spread from other sites - usually lung (45%) breast (20%)
-poor prognosis
Agents of CNS infection
bacteria, viral, protozoal, fungal
-acquired by direct extension via the blood, through the blood and via nerves
Common bacterial causes of CNS infection:
N. meningitidis (meningococcus) and S. pneumoniae, E. coli, H. influenzae, T. pallidum
Common viral causes of CNS infection:
measles, rubella or adenovirus, CMV, herpes virus, rabies virus, arbovirus (mosquito vector) resulting in various forms of encephalitides (St. Louis, California, Venezuelan, etc), HIV, west Nile Fever, Dengue Fever
Mad Cow Disease
at least 2 forms of prions have been identified
-spread in animals by feed infection with neural tissues of infected animals
-brain has spongy appearance
infection of brain parenchyma; usually viral invasion of neural and glial cells
inflammation of the meninges
Viral Meningitis
T-lymphocytes fight virus --> exudate rich in T cells in subarachnoid space and CSF
-NO change in glucose
Bacterial Meningitis
exudation of neutrophils into subarachnoid space and CSF
-LESS glucose (it is used by the bacteria)
-S&S: stiff neck (nerves irritated by the infection)
Multiple Sclerosis
demyelinative disease affects 250,000 Americans, usually women 20-45 of Northern European origin who live in temperate climate zones above the 40th parallel
-clustering (NW Ohio)
Clinical Features of MS
recurrent episodes of neurologic symptoms
-sensory (touch) and motor (weakness) abnormalities
-Dx 2 separate sets of CNS symptoms

*Upper motor neuron injury
+Babinski, hyperreflexes
Pathology of MS
lesions infiltrated with T cells and macrophages in PLAQUES, oligodendroglial cells are gone (no insulation)
-Tx with corticosteroids, immunosupressives to SLOW
Neurodegenerative diseases
neuron cells themselves die (different from MS)
– Parkinson’s
– Huntington’s
– Alzheimer’s
form of dementia - atrophy of the corticol parts of the frontal and temporal lobes
-50-60% of people over 85
-loss of brain neurons that use acetylcholine as a transmitter affected
-LONG course, die from some other disease
-Dx only with exam of cortex so Dx is with the presence of progressive dementia
-subcortical (other than the cortex) neurodegenerative disorder
-movement disorders; decreased numbers of dopaminergic neurons in the substantia nigra – a part of the midbrain
-tremor, rigidity, bradykinesia postural instability
utosomal (chromosome 4) dominant neurodegenerative disease characterized clinically by choreiform movements and progressive dementia. (Chance 50/50 of getting)
-atrophy of the cortex and subcortical basal nuclei (caudate and putamen)
-appears in the 40s and rapidly deteriorates
- irregular, spasmodic involuntary movements of the limbs or facial muscles often accompanied by hypotonia (decreased muscle tone)

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