Nervous System

Question 0

What are clinical manifestations of increased ICP?

Answer 0

Diminished cognitive functioning, headache, N/V, seizures, papilledema (edema of the optic disk) causing blurry vision, unsteady gait, loss of sphincter control

Question 1

What are 2 mechanisms that can cause brain cell death?

Answer 1

Anaerobic metabolism

Deterioration of ion gradients

Question 2

How does anaerobic metabolism lead to cell injury and death?

Answer 2

Mitochondrial dysfunction -> anaerobic glycotic pathways -> pyruvate coverts to lactate -> H ions lead to acidosis affecting neuronal integrity (cell membrane) -> deterioration of ion gradients -> K leaves, Na, Cl, and Ca enter the cell leading to edema (water follows Na), injury and death

Question 3

Excessive glutamate can be released because of impaired membrane integrity. How can too much glutamate lead to cell injury/death?

Answer 3

Glutamate binds to NMDA receptor, allowing calcium to enter the cell. Too much calcium can kill it
NMDA receptor activation stimulates nitric oxide production, can lead to free radicals and reactive nitrogen species

Question 4

What is reperfusion injury and what does lipid peroxidation lead to?

Answer 4

When oxygen reenters cells, it can produce reactive oxygen products that behave as free radicals
Cell membranes may undergo lipid peroxidation which will impair cell membrane, this predisposes the cell to inflammation and more free radicals

Question 5

What is brain herniation? What is it caused by? How can it be assessed early?

Answer 5

Protrusion of brain tissue through an opening in the supporting dura of the brain. Caused by increased ICP.
Early assessment check pupil reflex (CN 2/3). Changes in size, shape, reactivity is an early indicator of increased ICP and possible brain herniation. Eye movements (CN 3,4,6) can also be affected by increased ICP.

Question 6

What are ways to check Oculovestibular reflex?

Answer 6

Doll’s eyes
Cold calorics test
Absence of reflex indicates brainstem dysfunction

Question 7

Primary traumatic brain injury: Focal vs. polar vs. diffuse?

Answer 7

Focal: localized to site of impact
Polar: due to acceleration-deceleration impact resulting in double injury (opposite to focal injury)
Diffuse: Widespread axonal injury due to movement of brain in the skull

Question 8

Concussion vs. Contusion

Answer 8

Concussion: mild TBI, alteration/loss of consciousness less than 30 min, **no damage on CT, symptoms: headache, N/V, dizzy, fatigue, blurred vision, cognitive/emotional disturbance
Contusion: CT/MRI reveals an area of brain tissue damage (necrosis, laceration, bruising)

Question 9

Intracranial Hematoma: Epidural vs. subdural vs. subarachnoid
Which effect veins/arteries?

Answer 9

Epidural: arterial injury, rapid onset of symptoms, followed by a period of normal cognition, then consciousness deteriorates again
Subdural: Involves bridging veins, slower onset, increased ICP 2-10 days later
Subarachnoid: rupture of bridging veins, blood spreads to CSF causing meningeal irritation, hydrocephalus, vasospasms, ischemia

Question 10

What is secondary injury of TBI?

Answer 10

Body’s response to initial injury which may cause more harm, includes ischemia, hypoxia, vasogenic/neurogenic edema increasing ICP, vessels may re-bleed or spasm

Question 11

What is the most likely cause of hemorrhagic stroke? Where does it normally occur?

Answer 11

Hypertension
Occurs within the brain parenchyma (supportive brain tissue), usually in the basal ganglia or thalamus
Morbidity/mortality is higher in hemorrhagic than ischemic

Question 12

Homonymous Hemianopsia: Know where blindness would be based on where lesion is. R optic nerve lesion, midline chiasm lesion, R perichiasm lesion, R optic tract lesion
Review picture on slide 50

Answer 12

Lesion on R optic nerve: R eye blind
Midline chiasm lesion: blind periphery
R perichiasm lesion: R nasal blindness
Lesion on R optic tract: L homonymous hemianopia (blind on L half of both eyes)

Question 13

Broca vs. Wernicke’s aphasia?

Answer 13

Broca: “BE” = broca expressive aphasia, poor articulation and vocabulary
Wernicke’s: Receptive aphasia, impaired auditory comprehension and speech that doesn’t make sense

Question 14

What are the most common causes of subarachnoid hemorrhage?

Answer 14

Cerebral aneurysms and AVMs (arteriovenous malformations)

Question 15

Where do most cerebral aneurysms occur?

Answer 15

Sacular/berry aneurysms are most common at areas of bifurcation in the circle of Willis (this is where flow is more turbulent)

Question 16

What are symptoms and treatment of cerebral aneurysm?

Answer 16

Symptoms: sudden severe headache with meningismus (triad including photophobia, N/V, and stiff neck)
Treatment: surgery- clipping or embolization, vasospasm managed by keeping blood volume and pressure normal to high and calcium channel blockers

Question 17

What is arteriovenous malformation?

Answer 17

Failure of capillary system to develop. Arterial blood is shunted to venous system and vessels enlarge, making a high risk of rupture and hemorrhage
Leads to seizures and neurological dysfunction

Question 18

What is meningitis?

Answer 18

Bacteria (most common is streptococcus pneumoniae) enters and colonizes in the nasopharynx, then moves to blood and CSF
It damages the BBB causing edema and increased ICP and neuronal necrosis
The big problem is the accumulation of neutrophils because they degranulate and destroy brain tissue, nerves, and vessels
Diagnostics will show increased neutrophils in the CSF during an LP

Question 19

What is encephalitis?

Answer 19

Inflammation of the brain caused by a virus which attacks the arachnoid and CSF via the respiratory or GI tracts or inoculation by insect bites

Question 20

What is a brain abscess composed of?

Answer 20

The core of the abscess is infected full of neutrophils and tissue debris. Fibrous gliosis form due to immune response on glial cells creating scar tissue

Question 21

How can anticonvulsants help people with seizure disorders?

Answer 21

People with seizure disorders have hyperactive or hypersensitive neurons. Anticonvulsants can target Na or Ca channels or enhance GABA

Question 22

What are some pathologic features of Alzheimers?

Answer 22

Degeneration of neurons in temporal and frontal lobes, brain atrophy (synapse loss, neuron loss), amyloid plaques (A-beta 42 causes aggregation), neurofibrillary tangles (tau proteins)

Question 23

With Alzheimers, will CSF Amyloid-beta 42 increase/decrease? Will tau in CSF increase/decrease? Will FDG (shows glucose metabolism) increase/decrease?

Answer 23

CSF A-beta 42 DECREASES (if it is not in the CSF, it is in brain tissue causing aggregation)
CSF Tau INCREASES (it normally does not dissociate to form insoluble tangles, should not be in CSF)
FDG DECREASES (decrease in synaptic activity)

Question 24

How is E4 allele of ApoE gene a risk factor of Alzheimers?

Answer 24

It modulates metabolism, aggregation, and clearance of Amyuloid-beta peptide

Question 25

As amyloid-beta increases, what happens to number of neurons and synapses?

Answer 25

Number of neurons/synapses DECREASE

Question 26

What is Dementia - Vascular Cognitive Impairment? (differs from Alzheimers)

Answer 26

Syndrome due to stroke or brain injury effecting cognition, white matter
Starts with endothelial dysfunction, this decreases autoregulation, demyelination and leads to neurovascular dysfunction

Question 27

Delirium vs. Dementia

Answer 27

Delirium: acute, abrupt onset, overactive autonomic nervous system
Dementia: progressive failure of cerebral function, gradual onset, nerve cell degeneration and brain atrophy, old age

Question 28

What is Parkinson’s? What are some factors present in Parkinson’s disease?

Answer 28

Degeneration of dopaminergic neurons in the substantia nigra and development of Lewy bodies in dopaminergic neurons
Factors: Inflammatory bodies leading to free radicals, excitotoxic pathways, mitochondrial dysfunction, neurotrophic factors (GDNF), and neuronal dysfunction/death

Question 29

Parkinson’s has no cure but what treatments help with symptoms?

Answer 29

Dopamine precursors, dopamine agonists, MAOIs, anticholinergics, antidepressants

Question 30

What is multiple sclerosis?

Answer 30

Inflammatory demyelinating disease of the CNS that affects young adults, autoimmune, causes inflammation and scarring of the myelin sheaths, slowly progressive
autoreactive T cells (B cells affected too), oligodendrocytes damaged

Question 31

What are symptoms and treatment of MS?

Answer 31

Exacerbations (heat, infection, trauma, stress) and remissions
Symptoms: double/blurred vision, weakness, poor coordination, sensory deficits, bowel/bladder incontinence, memory impairment
Tx: No cure but short-term steroid therapy may be helpful during acute exacerbations

Question 32

What is Amyotrophic Lateral Sclerosis? What are the mechanisms, symptoms, and treatment?

Answer 32

Progressive disease affecting upper and lower motor neurons
Symptoms: Weakness and wasting of uppers first, then impaired speech, swallowing and breathing, hyperreflexia in weak extremity
Patho mechanisms: excitotoxicity (glutamate, Ca), oxidative stress, mitochondrial dysfunction, neuroinflammation
Treatment: no cure (die in 3-5 years), glutamate inhibitor, riluzole

Question 33

What are the mechanisms of spinal cord injury?

Answer 33

Flexion
Hyperextension
Compression

Question 34

Spinal shock vs. neurogenic shock

Answer 34

Spinal shock: occurs immediately, temporary loss of reflexes (spasticity, flaccidity)
Neurogenic shock: cervical or upper thoracic injury, loss of brainstem and SNS control (symptoms: hypotension, bradycardia, resp failure)

Question 35

Describe autonomic dyreflexia

Answer 35

Secondary complication of spinal cord injury at or above T6
Sympathetic response increases BP, baroreceptors sense and activate PSNS leading to peripheral vasodilation, there’s an imbalance of SNS and PSNS

Question 36

What is Guillain-Barre Syndrome? Symptoms?

Answer 36

Inflammatory demyelinating disease of the peripheral nervous system (B and T cell mediated)
Symptoms: progressive weakness and diminished/absent myotatic reflexes (muscle contraction in response to stretch). The weakness starts in lower extremities and spreads to proximal spinal neurons
One form of GBS is AIDP (acute inflammatory demyelinating polyneuropathy)

Question 37

What is the treatment for Guillain-Barre Syndrome?

Answer 37

Plasmapheresis and immunoglobulin (this will activate the complement system and the bad B and T cells that are attacking the body)