BIO 271 Study Questions: Nervous System: (Part I & II)

Stroke:
● Infarction of brain tissue due to interference with blood supply
● Ischemia
○ Local ischemia – often due to blockage
■ Local damage and manifestations depending on cerebral artery involved
○ Global cerebral ischemia
■ Often secondary to cardiac arrest or shock
■ Impaired perfusion of entire brain
● Loss of function and generalized cerebral edema
■ Brain death if not reversed quickly
○ Risk factors
■ Diabetes, hypertension, hyperlipidemia, smoking, atherosclerosis
■ Heart disease
● Emboli from MI, atrial fib, endocarditis, prosthetic valves
■ Increasing age - arteriosclerosis
● Age > 65
■ History of TIAs
■ Obesity
■ Obstructive sleep apnea
■ Combination of oral contraceptives and cigarette smoking
● Hemorrhage
○ Interrupts blood supply to particular area
■ Causes local ischemia (local symptoms)
○ Bleed also causes Inflammation & Increased ICP
■ Will cause additional generalized symptoms
○ Risk factors
■ Hypertension
■ Anticoagulant therapy
■ Congenital malformation of blood vessels (aneurysms) increase risk for
hemorrhagic stroke
What is a TIA?
● temporary focal neurologic deficit with absence of infarction on neurologic imaging
● symptoms are present for minutes usually approximately 30-60 mins

Complete the chart:

Thrombotic CVA Embolic CVA Hemorrhagic CVA
Predisposing/ ● atherosclerosis ● atherosclerosis ● hypertension-
Risk factors in a cerebral (carotid artery) or arteriosclerosis
artery systemic source
(heart)

Signs and ● gradual may be ● Onset: Sudden ● Onset: sudden often

symptoms preceded by ● Increased ICP: occurs with activity
transient minimal ● Increased ICP: present
ischemic attacks often high
● increased ICP is
minimal

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 Effects on ● localized: may be ● Localized unless ● rupture of cerebral
Intracranial less permanent multiple emboli are vessel
pressure damage if present ● widespread and severe
collateral often fatal
circulation has
been established

Describe the typical symptoms found in an ischemic stroke involving the Middle Cerebral
Artery?
● Contralateral muscle weakness and sensory deficit
○ Usually upper body and UE
● Aphasia, dysarthria – if dominant cerebral hemisphere is affected (usually left hemisphere)
● Loss of spatial skills if right cerebral hemisphere is affected
● Note: inset reminder acronym: FAST

What symptoms will the patient experience if Broca’s area is damaged?

● Difficulty with speech and forming words

What symptoms will the patient experience if Wernicke’s area is damaged?

● aphasia and having trouble understanding words

Meningitis/ Encephalitis
What are the signs and symptoms of meningitis?
● Clinical manifestations – due to irritation/inflammation of meninges and increased
intracranial pressure
● Presentation is similar for bacterial and aseptic meningitis but bacterial meningitis are
generally more severely ill-appearing
○ Vomiting
○ Irritability & lethargy
○ Fever and chills
○ Severe headache
○ No focal signs
○ Back pain
○ Leukocytosis
○ Photophobia
● Specific signs of meningeal irritation
○ Nuchal rigidity
○ Brudzinski’s sign (neck flexion causes flexion of the hip and knee)
○ Kernig’s sign (resistance to leg extension when laying with hips flexed)
● Signs and Symptoms
○ seizures
○ signs of increased ICP
■ herniation
○ may have skin rash - depends on etiology
■ widespread petechial rash or purpura may be seen with meningococcal
disease

Which pathogens are more prevalent in each age group?

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 ● Children and young adults
○ Neisseria meningitidis aka meningococcus (gram –ve diplococci)
■ Classic meningitis pathogen
■ Frequently carried in the nasopharynx of asymptomatic carriers
■ Spread by respiratory droplets
■ Vaccine preventable
■ Epidemics can occur in unvaccinated communities
● Young children
○ Haemophilus influenzae (vaccine preventable)
● Older adults
○ Streptococcus pneumoniae – major cause (vaccine available)

What part of the nervous system is infected with encephalitis?

● Parenchyma of the brain and spinal cord can include meninges

Is encephalitis more commonly bacterial or viral?

● Viral

Complete the table

Pathogen Poliomyelitis Zoster (shingles) Tetanus
Pathophysiology ● Polio virus ● Caused by ● Due to toxin
● Immunizati reactivation of produced by
on available varicella-zoster anaerobic gram
● Endemic in virus in adults (V-Z positive
West and dormant in a nerve bacterium
Central after varicella) Clostridium
Africa; ○ Onset - tetani
● Highly years after ● Spores can
contagious primary survive in soil
● Direct infection of (years)
contact or varicella ● Wound infection
oral droplet (chickenpox can be source
● Fecal-oral ) for bacteria to
route enter body and
● Attacks begin toxin
motor production
neurons of exotoxin
the spinal
cord and
medulla
oblongata
Symptoms & ● Fever, ● Rash erupts in ● Exotoxin enters
Signs headache, distribution of one nervous system
vomiting, cranial nerve or one ● Tonic muscle
stiff neck, dermatome spasms
pain, flaccid ● Pain, paresthesia, ● Jaw stiffness
paralysis vesicular rash ● Difficulty
○ If antiviral swallowing
drugs are ● Stiff neck
started ● Headache and

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 within 48 skeletal muscle
hours of spasm
onset, pain ● Respiratory
is failure
significantly
reduced
● Lesions and pain
persist for several
weeks
○ Postherpetic
pain may
persist for
months to
years in
some cases.
● Vaccine available
for those 60 years
or older
○ Zostrix

Guillain-Barre Syndrome:
Discuss the etiology, pathophysiology and manifestations of Guillain-Barre syndrome.
● Also known as Post-Infection Polyneuritis
● Inflammatory condition of the PNS
● Etiology unknown
○ Linked to abnormal immune response following:
■ Viral infection
■ Immunization
● Pathophysiology
○ Inflammation of nerves resulting in demyelination and destruction of axons in
peripheral nervous system
○ Impairs nerve impulse conduction
■ Motor function – progressive weakness
■ Sensory function – affected but not as pronounced
○ If neuron cell body is undamaged then
■ can see regeneration of axon/myelin
○ Disease progresses in 3 stages
■ Acute/initial period ~1-4 weeks
■ Plateau period ~ few days – 2 weeks
■ Recovery phase ~ 4-6 months
● Signs and symptoms
○ Ascending flaccid paralysis
■ Inflammation begins in peripheral nerves of lower extremities and ascends
to involve trunk, neck and may involve cranial nerves
■ Progressive ascending muscle weakness, lack of reflex response, ascending
flaccid paralysis
■ Areflexia is the characteristic neurologic finding
■ Paralysis may move upward – vision and speech may be impaired
○ Involvement of diaphragm, respiratory muscles and muscles of swallowing
■ May require ventilator

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 ■ Feeding tube
○ Process may occur rapidly over a few hours or several days.
○ Dysautonomia may occur triggering labile BP and arrhythmias

Head Injury/Subarachnoid Hemorrhage:

Define:
a. Concussion (mild traumatic brain injury)
a. Reversible interference with brain function
b. Caused by sudden excessive movement of the brain
i. Shearing effect on tissue disrupts neuronal function
c. Often leads to loss of consciousness
d. Amnesia and headaches may follow
i. Recovery usually within 24 hours without permanent damage
ii. Repeated concussions may result in permanent damage
b. Contusion
a. Bruising of brain tissue, rupture of small blood vessels, and edema
b. Blunt blow to the head
i. Possible residual damage
ii. More severe force than with concussion

What are the characteristic findings that would raise concern for the presence of a basilar skull
fracture?
● otorrhea or rhinorrhea
● leaking CSF from ear or nose pathway for microbes to enter CNS
Complete the table:
Epidural Subdural Hematoma Subarachnoid
Hematoma Hemorrhage
Common results from develops between dura occurs in space between the
etiologies bleeding between and arachnoid arachnoid and pia mater
dura and skull -
middle meningeal
artery

? artery or artery vein artery

vein
? presents signs of trouble can be acute (signs Acute
acutely or arise within within 24hrs) or
delayed hours of injury subacute (increasing
onset of when the person ICP develops over a
signs/sx loses week or so). A chronic
consciousness subdural hematoma
after a brief may occur only in an
period of elderly person in
responsiveness whom brain atrophy
allows more space for a
hematoma to develop
Presenting SAME SAME ● General signs of
signs and increased ICP

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 symptoms ● Headache
● Nausea & Vomiting
● Confusion / may see
change in level of
consciousness
● All subtypes of
hematoma will lead to
local pressure on
adjacent tissue
● Seizures may occur
● Cranial nerve
impairment may occur
● Otorrhea or rhinorrhea
may be seen with basal
skull fractures
● (i.e. Leaking of CSF from
ear or nose) - Pathway
for microbes to enter
CNS
● Otorrhagia
● Blood leaking from ear
seen with temporal
bone fracture
● Fever
● May be sign of
hypothalamic
impairment or cranial
or systemic infection
Spinal Injury:
Describe the stage of Spinal Shock. Include this information: Is the paralysis seen at this stage
flaccid or spastic? Are the skeletal muscle reflexes increased or decreased during this stage?
● Occurs initially after spinal cord injury
● On average lasts days to weeks
● Conduction of impulses ceases at level of lesion, below level of lesion, and slightly above
level of lesion
○ Loss of all sensory and motor function below lesion
■ Areflexia (no sensory, skeletal muscle or autonomic reflexes)
■ Flaccid paralysis of skeletal muscles
● ANS is affected
○ Low/Unstable BP
○ Loss of bladder and bowel control

What are the findings seen during Recovery from Spinal Shock? Include this information: Are the
skeletal muscle reflexes increased or decreased during this stage AND why? Is the paralysis spastic
or flaccid?
● Spinal shock terminates after days to several
● Recovery is indicated by the gradual return of reflex activity below the level of the injury
○ Hyperreflexia will be seen because the normal inhibitory or “dampening” responses
cannot reach the cord level below the injury
● Inflammation gradually subsides

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 ○ Damaged tissue removed by phagocytes
○ Scar tissue formation
● If complete cord transection then voluntary motor activity and sensory impulses are
blocked at and below the level of damage
○ Spastic paralysis
○ Neurogenic bladder
○ Bowel incontinence

Describe in detail the triggers for and the events seen with autonomic dysreflexia. (injury at T6
or above)
● Stimulation of the Sympathetic Nervous System results in this massive autonomic system
reflex response
● Noxious stimuli to receptors below level of cord damage stimulates SNS – higher brain
cannot control the sympathetic outflow
● Examples of stimuli that can trigger an episode of autonomic dysreflexia:
○ Distended bladder or rectum
○ Stimulation of skin or pain receptors
■ Decubitus ulcer
○ Often initiated by infection, genital stimulation, or other stimuli
● Initially see excessive Vasoconstriction with increase in BP
○ HA
○ Visual impairment
● Elevated BP stimulates baroreceptors resulting in activation of parasympathetic nervous
system
○ Bradycardia
○ Vasodilation above the injury
○ Continued vasoconstriction below cord injury – message can’t be transmitted
through damaged cord level
● Autonomic Dysreflexia is a Medical Emergency
○ Control BP
○ Remove noxious stimulus that triggered the reflex

What level of spinal cord injury is associated with autonomic dysreflexia?

● Paraplegia

Define:
a. Quadriplegia
a. paralysis of all 4 extremities
b. Paraplegia
a. paralysis of the lower part of the trunk and legs

Hydrocephalus:
Define hydrocephalus:
● Hydrocephalus:“water on the brain”
○ Excess cerebrospinal fluid (CSF) accumulates within the ventricles and
subarachnoid space
● Pathophysiology
○ Increased volume of CSF leads to compression of brain tissue and blood vessels
○ Increased ICP

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Explain the difference between communicating versus non-communicating hydrocephalus
● Non-communicating hydrocephalus
○ the flow of CSF through the ventricular system is blocked usually at the level of the
■ Cerebral Aqueduct or at
■ Foramen of Monro
○ Usually results from a fetal developmental abnormality
■ Stenosis or atresia
■ Neural tube defect
● myelomeningocele
■ Arnold-Chiari malformation
● Herniation of cerebellar tonsils
○ Obstruction from tumors, infection, scar tissue may occur at any age
■ Meningitis during acute illness
○ Obstruction leads to back pressure of fluid in the ventricles
■ Increased ICP
■ Ventricles enlarge and compresses blood vessels and brain tissue
● Communicating Hydrocephalus
○ Overproduction of CSF – rarely
○ Defective absorption of CSF – most common
■ Absorption of CSF through subarachnoid villi is impaired – often due to
inflammation and scarring
● Fibrosis in meninges from meningitis
○ Pathway between ventricles and subarachnoid space is intact

Spina Bifida:
Define spina bifida:
● A group of neural tube defects. It is a common developmental abnormality
○ Note: The neural tube develops during the 4th week of gestation
● Basic defect = Failure of the posterior spinous processes on the vertebrae to fuse
○ May permit meninges and spinal cord to herniate
○ May result in neurologic impairment
● Most common location – lumbar area

What are the three categories of defects seen in spina bifida? Explain the anatomical difference
between each of the three types of defects:
● Spina bifida occulta
○ Spinous processes do not fuse BUT
○ Herniation of spinal cord and meninges does not occur
○ Defect may not be visible
■ A dimple or a tuft of hair on the skin may be seen over the site
○ Diagnosed by:
■ Routine radiograph
■ May be asymptomatic or
■ May have mild neurologic signs that manifests as child grows
■ However, there is usually no significant impairment of function
● Meningocele
○ Herniation of the meninges occurs through defect
○ Meninges and CSF form a sac on the surface
○ However, there is no neural tissue present in the herniation
○ Trans-illumination confirms absence of nerve tissue in sac

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 ○ Usually no neurological impairment unless complications occur - such as
■ Infection
■ Rupture of the sac
● Myelomeningocele
○ Most serious form
○ Herniation of spinal cord and nerves along with meninges and CSF
○ Considerable neurologic impairment
■ Motor function
■ Sensory function
■ Bowel
■ Bladder
○ Degree of neurologic impairment is related to amount and location of herniated
neural tissue
○ This defect is often associated with hydrocephalus

A deficiency of which of the B group vitamins is thought to contribute to an increased risk of

neural tube defects?
● Folic acid

Cerebral Palsy:
Define Cerebral Palsy:
● Group of disorders marked by motor impairment:
● All individuals with have some degree of motor impairment
● Non-progressive – “static”
○ Damage may occur before, during, or shortly after birth
● May also see impaired mental functioning
○ Other areas of CNS may be affected
■ Gives varying clinical picture

List possible etiologies for Cerebral Palsy:

● Single or multiple factors
● Genetic mutations
● Structural brain abnormalities
● Infection
● Hypoxic brain damage
○ Hypoxia or ischemia – causes major brain damage
■ Intrauterine, perinatally or postnatal
■ Placental complications, difficult delivery, vascular occlusion, hemorrhage,
aspiration, respiratory impairment in premature infant
● High bilirubin levels – kernicterus
○ Accumulated bilirubin crosses blood brain barrier and damages neurons
● Metabolic abnormalities
○ Hypoglycemia in mother or child

Seizure Disorders:
What is a seizure?
● uncontrolled excessive discharge of neurons in the brain

Define Status Epilepticus:

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 ● Convulsive Status Epilepticus is defined as a generalized tonic-clonic seizure lasting more
than 5 minutes, or two GTCS occurring within 5 minutes of each other without a return to
baseline mental status.
○ Damage can occurs to neurons from hypoxia, hypoglycemia, acidosis and
hypotension
● Status Epilepticus is a Medical Emergency

Seizure disorder can be primary or secondary to some other illness. List some secondary causes of
seizures:
● Seizures may result from an abnormality in the brain or from systemic causes
● May be a temporary problem (seizure)or chronic and frequent (epilepsy/seizure disorder)
● Seizures may result from an abnormality in the brain or from systemic causes
● Metabolic derangements
○ Electrolyte imbalance
○ Hypoglycemia
● High fever
● Trauma
● Tumor
● Hemorrhage, CVA
● Hypoxia
● Drugs – ETOH withdrawal

Name the two types of generalized seizures that were discussed in lecture:
● Generalized seizures –
○ Have multiple foci or origins in structures of cerebral hemispheres and brainstem
○ Cause loss of awareness or consciousness
● Partial seizures
○ Single or focal origin
■ Often in cerebral cortex
○ Categorized as
■ Simple
● No LOC
■ Complex
● May involve altered consciousness
● May progress to generalized seizures

Describe the sequential stages of a tonic-clonic seizure (i.e. grand mal seizure)
● Characteristic pattern
○ Prodromal Phase:
■ Nausea, irritability, depression, muscle twitching
○ Aura –
■ Peculiar visual or auditory sensation which precedes LOC
○ Loss of consciousness is seen
■ Loss of postural reflexes and person falls to the ground
○ Tonic Stage
■ Strong tonic muscle contraction
■ Brief flexion, followed by extension of limbs
■ Rigidity in the trunk
■ The onset of this phase is often associated with a cry or a moan
■ Respiration ceases

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 ○ Clonic stage
■ Muscles alternatively contract and relax, violent generalized shaking
● Repetitive jerking movements of the body
■ Tongue may be bitten
■ Hypoxia usually develops – cyanosis
■ Increased salivation and loss of bowel/bladder control may occur
■ Breathing resumes at the end of this phase
○ Postictal stage
■ Limp / Lethargic / Confused
■ Typically falls into a sleep state
■ Amnestic for seizure

Describe a typical absence seizure (petit mal): (Is an absence seizure generalized or partial?)
● Absence seizures are also a type of generalized seizure
● More common in children than in adults
○ onset around 5 years of age
● Brief loss of awareness/consciousness
○ Lasts for 5 to 10 seconds
○ Staring episodes
○ May be associated with involuntary movements – automatisms
■ facial movement
● Lip smacking
● Eyelid twitches
■ Picking at clothes
● No memory of episode
Complete the table:

Multiple Sclerosis ALS Myasthenia Gravis

Etiologies ● Multiple Sclerosis is ● Also referred to as Lou ● Chronic degenerative
/ characterized by progressive Gehrig disease, (and aka disease affecting NM
Pathophy demyelination of axons in the motor neuron disease) junction and skeletal
siology brain, spinal cord, and optic ● Progressive degenerative muscle function
nerves disease affecting upper ● Autoimmune disorder
○ Loss of myelin motor neurons (cell ● Auto-antibodies to
○ See diffuse pattern of bodies in the cerebral ACh receptors at NM
involvement cortex) and lower motor junction block
○ Disease is marked by neurons (cell bodies in binding site for
exacerbations and brainstem and spinal acetylcholine
remissions but leads cord) ○ Prevents
to progressive ○ Spares sensory skeletal
deterioration neurons, CN III, IV, muscle
○ Different and VI stimulation
classifications of MS - ○ Cognition ○ Results in
variation in effects, unimpaired skeletal
severity, and ● More common in males muscle
progression ● Average age of onset ~ weakness and
■ Relapsing- 40-60years fatigue
Remitting - ● Etiology – idiopathic ○ Eventual
85% ○ Genes on various destruction of
■ Primary chromosomes receptor site

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 Progressive have been linked and changes
■ Secondary to the disease in NM
Progressive ■ Possible junction
■ Progressive- genetic ● Facial and ocular
relapsing defect in muscles usually
● Onset usually occurs between enzyme affected first
ages 20 and 40 peak age 30 superoxid ○ Followed by
● Women more commonly e weakness of
affected than males dismutase proximal arm
○ 2:1 ratio ○ ~10% of cases are and leg
● Autoimmune familial ○ Muscles of
● Thought to have genetic, ○ Possible respiration
immunologic, and neurotoxin may be
environmental components produced by affected in
○ Increased risk for astrocytes advanced
close relatives of ○ Most cases are cases
affected individuals “random”
● ? Viral infection may trigger ● Progressive destruction of
onset in genetically motor neurons in brain
susceptible individuals and spinal cord
● Immune system generates an ● Sensory function and ANS
inflammatory process in the function are usually not
CNS affected
○ Peripheral nervous ○ Does not affect
system is not affected sensory neurons
(except for function of ○ Does not affect
a few cranial nerves) neurons
● See scattered localized areas associated with
of demyelination and CN that control
destruction of EOM
oligodendrocytes and axons ● No indication of
○ Can involve gray inflammation
matter ● Loss of upper motor
○ Occurs in diffuse neurons in cerebral cortex
patches in the ○ Spastic paralysis
nervous system and hyperreflexia
● Loss of myelin interferes with ● Damage to lower motor
conduction of impulses in neurons
affected axons ○ Flaccid paralysis
○ May affect motor, ○ Decreased muscle
sensory, and tone and reflexes
autonomic fibers
○ Most commonly
affects optic nerves,
pyramidal tracts,
posterior columns,
periventricular areas
and brainstem nuclei
● Chronic lesions are known as
Plaques scars

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 ○ Larger areas of
inflammation and
demyelination
develop later and
become visible on
MRI
■ Frequently
plaques are
beside the
lateral
ventricles, or
in the
brainstem or
optic nerve
○ Plaques vary in size
S/S ● Manifestations are ● Progressive muscle ● Muscle weakness is
determined by areas of weakness and loss of fine hallmark of disease –
demyelination motor coordination worsens as day
○ Blurred vision usually begins in the progresses
○ Diplopia, nystagmus upper extremities - hands ● Muscle weakness in
○ Dysarthria, dysphagia ● Stumbling and falls are head area, face and
○ Paresthesia, (areas of common eyes initially
numbness, burning, ● Dysarthria develops ● Impaired vision
tingling) followed by impaired ○ Diplopia
○ Loss of coordination swallowing and ■ Ptosis
○ Progressive weakness respiratory function ○ Head droops
in legs ● Cognition remains intact ○ Difficult
■ paralysis ● Death usually occurs due chewing and
extends to the to respiratory failure swallowing
upper limbs ○ Typically about 2- ● Arm weakness
■ Corticospinal 5 years after onset ○ Problems with
tracts grooming, self
○ Bladder, bowel and care
sexual dysfunction ● Impaired respiratory
○ Chronic fatigue function
○ Changes in affect: ○ Difficulty
depression, euphoria removing
○ Cognitive changes secretions
○ Ventilatory
support may
be needed

Complete the table:

Parkinson’s Disease
Pathophysiology/c ● “Paralysis agitans”

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 haracteristic ● Progressive degenerative disorder
changes seen in the ● Pathophysiology
nervous system ○ Progressive degeneration in basal nuclei, secondary to loss of
dopamine producing cells in the substantia nigra of the
midbrain
○ Loss of dopamine leads to Imbalance between excitation(Ach)
and inhibition (dopamine) in basal nuclei
What are the three ● See excessive stimulation
most prominent ● See loss of inhibiting effect of dopamine on motor activity
symptoms we ● Lose refined, controlled, motor activity
discussed in class? ● Later signs and symptoms:
○ Tremors affect hands and feet, face, tongue, lips.
○ Increased muscle rigidity
■ Cogwheel rigidity
■ Difficulty initiating movements
○ Slow movements - bradykinesia
■ Lack of associated involuntary movements
○ Postural instability
■ Characteristic posture is stooped, leaning forward
○ Complex activities become slow and difficult, including
speaking and eating

Huntington’s Disease:
What is the pattern of inheritance of this disorder?
● autosomal dominant

What symptoms will the patient develop?

● Changes in personality, mood swings
● Intellectual impairment
○ Loss of problem solving skills
○ Leads to dementia
● Choreiform movements of arms and face
○ Rapid, jerky, movements

Will all carriers eventually develop symptoms?

● 50% of the children of an affected parent will develop the disorder

What is the age of onset of symptoms?

● 35-40 years

Is genetic testing available?

● genetic testing is available

Dementia:
What are the characteristic gross and microscopic findings in the brain of a person with
Alzheimer’s?
● Progressive cortical atrophy
○ Microscopically ----> Loss of cortical neurons
■ Neurofibrillary tangles
● Interrupt axonal flow

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 ■ Beta- amyloid plaques
● Disrupt neural conduction
● Gross anatomy
○ Thinning of gyri and widening of sulci / reduced volume of hippocampus bilaterally
○ Dilation of ventricles

What is the etiology of Creutzfeldt-Jakob Disease?

● Infectious agent = Prion -----> infectious proteinaceous particle which alters protein shape
and thus protein function
What is the typical clinical course Creutzfeldt-Jakob Disease? (Include the duration of the
incubation period and the typical manifestations once symptoms begin.)
● Pathophysiology
○ Plaques and vacuoles form in neurons (spongiform encephalopathy)
○ Destruction of neurons with rapidly progressive dementia
● Signs & Sx develop very quickly - over 6-12 months
○ Long incubation period of vCJD (years – probably decades)
○ Progressive dementia leading to death in 6 -12 months

Herniated Disc:
In terms of the anatomy of the disc: describe the pathophysiology of herniated disc and the general
manifestation of the disorder.
● Pathophysiology of Herniated Intervertebral Disk:
○ Nucleus pulposus protrudes through annulus fibrosis
■ Tear in annulus fibrosis may occur suddenly or develop gradually with aging
or obesity
○ Usually occurs as a result of degenerative changes in the intervertebral disk
○ Exerts pressure on spinal nerve
■ Sensory, motor, or autonomic function may be impaired
■ If pressure is prolonged, severe permanent damage may occur
○ Most common location
■ lumbosacral disks L4 to L5 or L5 to S1
■ Some herniations involve cervical disks

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