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Advanced Patho Test 1 > Test 4 Neuro > Flashcards

Test 4 Neuro Flashcards

1
Q

Central Nervous System (CNS)
441

A

Brain and Spine that’s it.

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2
Q

What are the Peripheral Nervous System (PNS) (4)
Divisions
441

A

Cranial & Spinal Nerves

Divided into:

Afferent: ascending pathways that carries signals from the periphery to the CNS

Efferent: descending pathways that carry signals to skeletal muscle or effector organs though impulses

Somatic: voluntary muscle control

Autonomic: internal environment control involuntarily. Divided into sympathetic and parasympathetic

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3
Q

What does a neuron do?
What are the parts of the neuron?
442

What are the three types of neuron?
444

A

Communicates information to other neurons, muscles and glands or tissues using synapses.

-Cell body (soma)
-Dendrites (branching fibers)
-Axon- may or may not be myelinated

Types:
1. Sensory
2. Associational (carry impulse from neuron to neuron, only
found in the CNS)
3. Motor

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4
Q

What are Nuclei
442

A

dense collections of cell bodies in the CNS, most cell bodies are in the CNS even if their axons extend into peripheral nerves

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5
Q

What are the types of Glial Cells (5)
What do they do?
Where do you find them? (CNS or PNS)
444-445

A
  1. Astrocytes: component of BBB, rapid transport for nutrients, SCAR forming implicated in seizures. CNS
  2. Oligodendroglia: formation of myelin sheath CNS
  3. Microglia: clear cellular debris, phagocytic, key immune cell in CNS
  4. Ependymal: lining for ventricles and choroid plexuses, produce CSF, CNS
  5. Schwann:
    –Myelinating- form myelin sheath in PNS, direct axonal regrowth and functional recovery in PNS
    –NON-myelinating- neuronal metabolic support and regeneration in PNS
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6
Q

Which neurotransmitters are classified as Monoamines?
447

A

Norepinephrine
Dopamine
Serotonin

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7
Q

Which neurotransmitters are Amino Acids?
447

A

Glutamate
Glycine
Gamma-amino-butyric acid (GABA)

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8
Q

What is the Corpus Collosum?

A

Separates right and left cerebral cortex

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9
Q

Lobes of the cerebral cortex?
What is each of their function?

A

Temporal: hearing, crude vision, smell, taste

Parietal: language, interpretation of somatic experiences, motor control, special relation and body position

Frontal: behavior, personality, abstract thinking, motor control, smell, speech

Occipital: vision, spacial orientation

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10
Q

What are the 3 parts of the Mid-Brain?
What are their functions?

A

Thalamus: relays impulses to and from the cerebral cortex, controls consciousness

Hypothalamus: regulates temperature, hunger and hormones

Reticular Activating System: consciousness sleep/wake cycles

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10
Q

What are Ganglia?
442

A

Dense groups of cell bodies in the PNS

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11
Q

What is myelin?
Who makes it?
What does it do?
What is the space between them called?
Why do we need that space?
442

A

-What is it?
Membrane of lipid material

-Who makes it?
In CNS made by oligodendrocytes where it’s called white matter
In PNS Schwann cells

-What does it do?
increase the speed of impulse transmission by allowing it to leap entire segments called SALTATORY CONDUCTION

-Space between?
Nodes of Ranvier

-Why?
Nutrients can’t penetrate the myelin
axons can branch there and form collaterals

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12
Q

$$$$$$$$

Acetylcholine
What does it do as a neurotransmitter?
Where does it work?
Excitatory or Inhibitory?
Clinical significance?

447 & Lecture

A

Controls muscle tone and gland secretion

Brain, spinal cord, neuromuscular junction of skeletal muscle, and many ANS synapses

Typically excitatory BUT inhibitory in parasympathetic nerve endings (vagal response)

-Alzheimer’s associated with acetylcholine.
-Myasthenia gravis autoimmune cells respond to acetylcholine receptor on postsynaptic terminal

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13
Q

$$$$$$$$

Norepinephrine
What does it do as a neurotransmitter?
Where does it work?
Excitatory or Inhibitory?
Clinical significance?
447 & Lecture

A

Controls mood, wakefulness, integration

brain, spine and some ANS

Excitatory (book says also inhibitory but doesn’t say what receptors or organs)

-CNS: Cocaine and amphetamines increase the release and block reuptake of norepi, overstimulating post synaptic neurons
-PNS: Sympathetic nerve stimulation

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14
Q

$$$$$$$$

Dopamine
What does it do as a neurotransmitter?
What areas does it exert influence?
Excitatory or Inhibitory?
Clinical significance?

447 & Lecture

A

Controls mood, integration and movement

Brain and ANS

Generally excitatory (book)
Inhibitory (lecture)
Google says it’s both depending on the neuron receptors

-Parkinson’s destruction of dopamine secreting neurons.
- Schizophrenia
-Drugs used to increase dopamine can induce vomiting and hallucinations
-part of positive feed back loop with addiction

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15
Q

$$$$$$$$

Serotonin
What does it do as a neurotransmitter?
Where does it work?
Excitatory or Inhibitory?
Clinical significance?
447 & Lecture

A

Mood, anxiety, and sleep induction

Brain and spinal cord

Generally Inhibitory

Levels of serotonin are elevated in schizophrenia

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16
Q

$$$$$$$

Glutamate
What does it do as a neurotransmitter?
What area does it exert influence?
Excitatory or Inhibitory?
Clinical significance?

447 & Lecture

A

Controls integration
-Lecture says released with TBI causing seizures

Brain and spinal cord

Excitatory

Drugs that block glutamate might prevent overexcitation from seizures and neural degeneration.

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17
Q

$$$$$$

Glycine
What does it do as a neurotransmitter?
Where does it work?
Excitatory or Inhibitory?
Clinical significance?

447 & Lecture

A

controls integration

Spinal cord

most postsynaptic inhibition in the spinal cord

glycine receptors are inhibited by strychnine (ingredient in rat poison)

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18
Q

$$$$$$$

Gamma-amino-butyric acid (GABA)
What does it do as a neurotransmitter?
Excitatory or Inhibitory?
Clinical significance?
447 & Lecture

A

controls wakefulness, awareness integration

most neurons in CNS have these receptors

MOST COMMON inhibitor in the brain

Drugs used to increase GABA function treat epilepsy by inhibiting excessive discharge of neurons

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19
Q

What 2 parts of the skull close in babies?
At around what age for each?

Lecture

A

Anterior fontanel
12-24 months

Posterior fontanel
2 months

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20
Q

What is the tentorium?
What structures are considered supratentorial & which infratentorial?
457 & Lecture

A

A membrane, used as a common landmark, that separates the cerebellum below from the cerebral structures above.

Supra= cerebrum
Infra= cerebellum

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21
Q

What are the cerebral cortex structures?
What are their functions?
449-450

A

-Right and left cerebral cortex divided by corpus collosum

-Frontal: Broca’s area (motor aspects of speech/expressive aphasia), behavior personality, abstract thinking, smell, motor control (homunculus is here)

-Parietal: somatic sensory, proprioception, motor, language

-Temporal: hearing, crude vision, smell and taste, Wernicke’s area (receptive aphasia)

-Occipital: vision, visual association

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22
Q

What are the layers of the cranial vault, including the brain (8)?
456-457

A
  1. Skin
  2. Periosteum- endosteal layer of the skull (outer dura)
  3. Bone
  4. Dura mater (inner)- rigid membranes that support and separate various brain structures
  5. Arachnoid- spongy web-like structure that loosely follows the contours of the cerebral structure
  6. Pia mater- adheres to the brain and spinal cord contours, provides support for blood vessels serving brain tissue
  7. Grey matter
  8. White matter
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23
Q

What is the thalamus?
Where is it located?
What does it do?
451-452

A

Major integrating center for afferent impulses to the cerebral cortex

Forebrain/diencephalon

Controls consciousness, Relay center for info from the basal ganglia and cerebellum to the appropriate motor area.

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24
Q

What is the hypothalamus?
Where is it located?
What does it do?
452

A

Small structure inferior to the thalamus, that exerts its function through the endocrine system and neural pathways

Base of the forebrain/diencephalon

maintain constant internal environment, implement behavioral patterns, control ANS function, regulate body temp, endocrine function (hunger etc), adjust emotional expression

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25
Q

What is the reticular activating system?
448

A

large network of diffuse nuclei connecting the brain stem to the cortex and controls vital reflexes
-cardiovascular function & respiration
-essential for maintaining wakefulness and attention (consciousness)

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26
Q

$$$$$$

What is the basal ganglia?
What does it do
450 & Lecture

A

group of nuclei that includes the caudate nucleus, putamen, and globus pallidus

-voluntary movement and cognitive and emotional function

-lecture says increase muscular tone & a primary symptom of injury to this area is increased tone

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27
Q

What is the Pons? What does it do?
453

A

A bulging appearance below the mid-brain

-transmits information from the cerebellum to the brainstem and between the two cerebellar hemispheres.
-The nuclei from the fifth - eighth cranial nerves are located here

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28
Q

What is the medulla? What does it do?
453

A

also called the myelencephalon forms the lowest portion of the brain stem.

Reflex activities (HR, respiration, blood pressure, coughing, sneezing, swallowing and vomiting.

Nuclei of cranial nerves nine- twelve are in this area

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29
Q

What part of the brain do the ANTERIOR CEREBRAL ARTERIES serve?
If there was an occlusion what symptoms would that cause?
461 & AO

A

bilateral basal ganglia, corpus callosum, medial cerebral hemispheres, superior surface of frontal and parietal lobes

-Hemiplegia on contralateral side
-urinary incontinence
-if L side may cause expressive aphasia

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30
Q

What part of the brain does the MIDDLE CEREBRAL ARTERIES serve?
If there was an occlusion what symptoms would that cause? 461

A

frontal lobe, parietal lobe, cortical surface of temporal lobe, Broca’s area, part of occipital

-aphasia in dominant hemisphere
-contralateral hemiparesis (UPPER> lower)
-head and eye deviation toward the side of the stroke
-LEFT: aphasia, possibly global
-RIGHT: possible apraxia, hemineglect
Lecture and Google: SAYS VISUAL AND SENSORY

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31
Q

What part of the brain does POSTERIOR CEREBRAL ARTERY serve?
If there was an occlusion what symptoms would that cause?
461 & AO

A

Part of diencephalon (thalamus, hypothalamus) temporal lobe, occipital lobe, cerebellum, parietal

-visual loss contralateral
-diplopia, hemianopia
-sensory loss
-contralateral hemiplegia if cerebral peduncle affected
-aphasia

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32
Q

What part of the brain does the VERTEBRAL- BASILAR ARTERIES serve?
lecture and google & AO

A

posterior occipital, cerebellum, brain stem, thalamus, medulla, pons

hemi or quadriparesis, loss or change in vision, confusion, AMS

-SWALLOW
-Speech
-loss of pain and temp sensation
-Muscle weakness
-balance/vertigo
-nystagmus
-N/V
-diplopia

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33
Q

Through what vessel does the majority of cerebral blood flow?
549

A

Paired carotid arteries

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34
Q

What vessels constitute the CIRCLE OF WILLIS (5)?
Why is the circle so important?
459-460 & lecture

A
  1. posterior cerebral arteries
  2. posterior communicating arteries
  3. internal carotid arteries
  4. anterior cerebral arteries
  5. anterior communicating arteries

-collateral circulation if occlusion occurs. though 5% of the population does not have an intact COW.
-assists in regulating differential blood flow to the brain
-shuts blood where it’s needed most based on current activity (ie thinking= frontal, running= motor cortex)

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35
Q

What is different in the blood brain barrier in infants?
Lecture

A

More permeable, increased risk for meningitis. As they get older the permeability decreases and fewer organisms can cross.

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36
Q

What are the properties of the blood brain barrier that make it so protective of the brain?
460

A
  1. endothelial cells in the brain capillaries have intracellular tight junctions (EXCEPT at the hypothalamus to allow for sensing)
  2. Only some substances: glucose, lipid-soluble molecules, electrolytes, and some chemicals can cross; is facilitated by transport molecules.
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37
Q

What is different about the cerebral venous system when compared to the arterial system that increases the risk of intracranial pressure?
460

A

Outflow does not match arterial inflow. Adequacy of venous outflow can significantly affect ICP.

If someone with a head injury turns their head or allows it to fall, this can partially occlude venous return causing an increase in ICP.

38
Q

What structure produces CSF?
How much is made/day?
What is the purpose of CSF?
458

A

choroid plexus in the lateral, third, and fourth ventricles produce the majority of CSF.

35mL/min or about 500mL/day

protection from jolts and blows, buoyant properties prevent the brain from tugging on meninges, nerve roots, and blood vessels.

Tight junctions in the choroid blood vessels provide a limiting barrier between CSF and the blood similar to the BBB.

39
Q

What is the Monro-Kellie Doctrine?
Why do we care?
Lecture & google
(book discusses the topic on 534 but I don’t see the name)

A

the total volume of the brain, cerebrospinal fluid (CSF), and blood within the cranium is constant. This means that if one of these components increases in volume, the volume of one or both of the other components must decrease.

Implications in ICP management, blood is the easiest and fastest to change. High ICP may not be symptomatic initially because of adequate compensation.

40
Q

What is normal Cerebral Perfusion Pressure (CPP)?
How is CPP calculated?
What is normal ICP?
534-535

A

70-90mmHg

MAP-ICP=CPP

5-15mmHg, >20-25 considered Increase Intracranial Pressure or Cranial hypertension

41
Q

What occurs in the four stages of elevated ICP?
What are the symptoms in each stage?
534-535

A
  1. Compensatory- vasoconstriction and external compression of the venous system occur to further decrease ICP.
    —-May be asymptomatic if effective.
  2. Early signs- high ICP exceeds the brain’s compensatory capacity. Pressure begins to compromise oxygenation, and systemic arterial vasoconstriction occurs to elevate the systemic blood pressure to sufficiently overcome the ICP.
    —–Symptoms: subtle and transient; episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes.
  3. Brain injury begins- ICP begins to approach arterial pressure, the brain tissues begin to experience hypoxia and hypercapnia and the patient’s condition rapidly deteriorates.
    —–Symptoms: decreased LOC, neurogenic hyperventilation, widened pulse pressure, bradycardia, and pupils become small and sluggish.
  4. Herniation- brain tissue shifts from the compartment of greater pressure to a compartment of lesser pressure. The shifted tissue’s blood flow is compromised causing further ischemia and hypoxia in herniating tissues.
42
Q

What are the 6 kinds of brain herniation?
535

A
  1. Uncal
  2. Central
  3. Cingulate/subfalcine
  4. Transcalvarial/extra cranial
  5. Upward herniation of cerebellum
  6. Cerebellar tonsil/cerebellum into foramen magnum
43
Q

What are the functions of the Autonomic nervous system (ANS)?
465 & lecture

A

-coordinates and maintains the steady state among body organs
-regulates cardiac muscle
-smooth muscle
- regulation of the body’s glands
-sweating
-piloerection
-visceral reflexes

44
Q

What are the segments of the spinal COLUMN?
Where does the spinal CORD start and end?
What is the cauda equina?
Clinical Significance?
453 & Lecture

A

Cervical 8
Thoracic 12
Lumbar 5
Sacral 5
Coccygeal 1

CORD originates in the medulla and ends at the first or second lumbar vertebra in adults.

Cauda equina= nerves that continue from the end of the spinal cord and form a nerve bundle.

Significance: when doing things like lumbar punctures it is always a good idea to do it below the spinal cord as it is much higher risk for injury. Thus lumbar.

45
Q

What do the anterior and posterior horns of the spinal cord do?
453

A

Anterior/ventral: Motor neurons (efferent). Carry motor stimuli to control skeletal muscles

Posterior/dorsal: Sensory neurons (afferent). Carry sensory signals back to the brain.

46
Q

What are the three clinically significant afferent (sensory) pathways?
457

A
  1. Posterior column- carries fine touch sensation, two pint discrimination and proprioceptive information.
  2. Anterior spinothalamic- vague touch, and pain
  3. Lateral spinothalamic- vague touch and temperature perception
47
Q

What is the pyramidal tract (lecture) corticospinal tract (book)?
Lecture & 456 & google

A

the main neuronal pathway that controls voluntary movement by connecting the cerebral cortex to the spinal cord.

48
Q

Age related changes in brain/spine both children and the elderly
Lecture

A

Children
-myelin develops into teenage years making recovery from injuries easier in children (plasticity)
-reflexes are marker of healthy nervous system development
-normal reflexes CHANGE AT FIRST YEAR

Elderly
-Decreased neurons, myelin and dendritic processes with synaptic connections therefore decrease in brain weight and size. CSF increases to fill the space.
-Increased arteriosclerosis
-Increased BBB permeability (increased risk of meningitis)
-functional changes: decreased deep tendon reflex, taste, smell or color detection; sleep disturbances, memory impairment.
—-These changes occur even in mentally competent people

49
Q

Define primary headache syndrome
What are the primary headache syndromes (3)?
597

A

Chronic, recurring type not associated with structural abnormalities, systemic disease, or trauma.

  1. Migraine
  2. Cluster
  3. Tension
50
Q

Define Migraine
What is the etiology?
What are common triggers?
What are the phases?

597-598

A

At least 5 attacks of a headache lasting 4-72 hours with at least two of the following characteristics: unilateral, pulsating, moderate or severe pain, and aggravation by or causing avoidance of routine physical activities.
Must have at least one of the following symptoms: nausea and or vomiting, photophobia and phonophobia and not be accounted for with another diagnosis.

Etiology: Combination of genetic and environmental

Patho unknown

Triggers: (things that decrease the threshold for headache) fatigue, oversleeping, missed meals, overexertion, weather change, stress or relaxation from stress, hormonal changes (menstruation), over stimulation (light, sounds, smells), chemicals (alcohol or nitrates).

Phases:
1. Premonitory: up to 1/3 of people get it, can be up to days ahead of time when they get pre headache symptoms.
2. Aura: up to 1/3 get it, up to 1 hour duration, visual sensory or motor.
3. Headache
4. Recovery: irritability, fatigue, or depression may take hours or days to resolve.

51
Q

What is a CLUSTER headache?
Symptoms?
Common sufferers?
Triggers?
Patho?
598

A

One in a group of disorders called trigeminal autonomic cephalalgias (headache involving the autonomic division of the trigeminal nerve) that usually begins without warning.

Sx: Unilateral (may alternate with each episode), severe, stabbing and throbbing pain. Occurs in clusters (up to 8 attacks in a day) and can last from minutes to days, followed by a long remission.

Primarily in men age 20-50

Triggers: Alcohol, caffeine and smoking

Patho: release of vasoactive peptides, neurogenic inflammation and pain activation.

52
Q

What is a TENSION headache?
Symptoms?
Common sufferers?
Triggers?
Patho?
598-599

A

Most common type of recurrent primary headache. Average onset is 20yo, associated with anxiety and depression.

Etiology:

Symptoms: bilateral and mild with sensation of tight band or pressure around the head with gradual onset of pain that can last from hours to days.
Episodic =less than 15 days/mo
Chronic = 15 or more days/mo x 3 months

Triggers: NOT aggravated by physical activity, triggered by sleep disorders (insomnia)

Patho: peripheral sensitization of myofascial nociceptors (not really known)

53
Q

What is Delirium?
Patho?
Typical onset?
525-526

A

Aka Acute confusional state, can be acute or chronic, sudden or gradual onset.

Patho: not well understood, possibly alteration in neurotransmitter availability and function. OR could be a failure in the function of neuronal networks that integrate and process sensory information. (Reticular activating system according to the lecture)

Usually develops over hours to days

Types:
-Hyperactive
-Hypoactive
-Mixed
-Terminal (seen in the final stages of dying)

54
Q

What is Dementia?
Cause?
527

A

Acquired deterioration and progressive failure of many cerebral functions including impairment of intellectual processes, decreasing ability in language, memory, judgement, and decision making.

SLOW

Cause: neuronal degeneration, compression of brain tissue, atherosclerotic vessels and brain trauma.

55
Q

What is Alzheimer’s Type Dementia?
Cause?
Mechanism?
528-534

A

LEADING cause of severe cognitive and behavioral dysfunction in older adults. (2/3 are women!!) BOO!!

Cause: exact not known, very likely genetic, many genes found to be possible especially with EARLY onset.

Mechanism:
-accumulation of extracellular neuritic plaques containing a core of abnormally folded beta amyloid proteins and tau protein neurofibrillary tangles
- loss of neurons and synapses in cerebral cortex and hippocampus.
-Atrophy with decreased overall brain weight and volume, loss of neurotransmitters.

NO GOOD TREATMENT

56
Q

What is BACTERIAL Meningitis?
Common offending pathogens?
How it occurs?
Symptoms?
Diagnosis?

600

A

Inflammation of the brain and spinal cord.
-Bacterial it is primarily an infection of the pia mater, arachnoid villi, subarachnoid space, ventricular system and the CSF.

-Agents: Streptococcus pneumoniae & Haemophilus influenzae type B (Hib)

-How: Respiratory droplets, contact with contaminated saliva or respiratory tract secretions. Carriers of the meningococcal bacteria can pass it on but are not infected by it.
—–Inhalation & crossing BBB

-Symptoms: normal inflammatory symptoms + throbbing HA, severe photophobia, nuchal rigidity and positive KERNIG (inability to/pain with extension of the legs past 90 degrees) AND BRUDIZINSKI SIGNS (passive flection of the neck causes flexion in the knees) IN SEVERE CASES CAUSES PROJECTILE VOMITING WITH NECK FLEXION

-Diagnosis: CSF with increased WBCs (neutrophils), positive polymorphonuclear leukocytes, low glucose and high protein.

57
Q

What is VIRAL Meningitis?
Common offending pathogens?
How it occurs?
Symptoms?
Diagnosis?

602

A

Aka aseptic meningitis, limited to the meninges and no identifiable bacteria can be found in the CSF

Agents: HSV 1&2, enterovirus (echo virus, coxsackievirus), arboviruses

How: crossing BBB itself, spread along peripheral nerves, though transsynaptic transmission, choroid plexus epithelium or infected immune cell crossing the BBB.

Symptoms: Similar to bacterial meningitis but MORE MILD

Diagnosis: R/O bacterial cause

58
Q

What is Encephalitis?
Common Agents?
Vectors?
Symptoms?
Diagnosis?
602-604

A

acute inflammation of the brain, usually of viral origin.

Agent: infectious, postinfectious or AUTOIMMUNE
—MOST COMMON INFECTIOUS HSV1
—CAN follow vaccination with live virus IF vaccine has an encephalitis component (ie mmr)

Vector: MOST COMMON bug bites (tick, mosquito and flies)

Symptoms: acute febrile illness with meningeal involvement.

Diagnosis: CSF typically “normal” serologic studies, CBC, CT

INTERESTING: There is a California viral encephalitis which is endemic!

59
Q

What is a seizure?
Causes?
Patho?
Most common kind in kids?
588-591

A

Sudden, transient disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons.

Causes: ANY disorder that alters the neuronal environment can cause seizure. (ie congenital malformations, brain tumors, vascular disease, drug/alcohol use, trauma)
—-Threshold decreased by hypoglycemia, fatigue, emotional or physical stress, fever, constipation, antipsychotics, HYPONATREMIA (like excess H2O intake)

***Lecture says Hyper & Hypo natremia can cause seizures, google agrees saying they do but they have different causes and treatments. The book says hyponatremia.
—-LECTURE: HYPERNATREMIA SEIZURE= HIGH TONE/HYPERREFLEXIA, where hypo is lethargy

Patho: Disruption in the balance of inhibitory and excitatory impulses.

Kids: Febrile

60
Q

What is status epilepticus?
Why is it such a problem?
590-591

A

a state of continuous tonic-clonic seizures lasting more than 5 minutes, OR rapidly recurring seizures before the person has fully regained consciousness from the preceding seizure, OR a single seizure lasting more than 30 minutes.

Causes severe increase cerebral metabolic demand using glucose and glycogen stores leaving cells HYPOXIC
–Neuronal death, injury and alteration of neuronal networks.

61
Q

What are the hallmarks of Parkinson’s Disease?
Primary vs Secondary?
547

A

Lewy Bodies
Decreased Dopamine generating cells
Resting tremor
Bradykinesia
Postural instability
Degeneration of the locus coeruleus causing decreased NOREPI -> depression and cognitive decline

Primary = disease (genetic/idiopathic)
Secondary= Acquired (drugs toxins, MS, cancer etc)
-DRUG INDUCED IS THE MOST COMMON SECONDARY AND IS USUALLY REVERSIBLE

62
Q

What is Multiple Sclerosis?
Cause?
Common sufferers?
Symptoms?
557-559

A

chronic immune medicated inflammatory disease involving degeneration of the CNS myelin, scarring (sclerosis or plaque formation), and loss of axons. Diffuse injury
–PROGRESSIVE OR REPLAPSING AND REMITTING

Cause: Autoimmune or post infectious (MONO) etiology unknown

Common: women 20-40, higher in northern latitudes and those who have less sun exposure.

Symptoms: MOST COMMON paresthesia of face, trunk, or limbs; weakness, impaired gait, or urinary incontinence. Vision changes.

63
Q

What is Myasthenia Gravis?
Common sufferers?
Give away symptom?
Treatment?
561-562

A

acquired chronic autoimmune disease mediated by antibodies against the ACETYLCHOLINE receptor at the POSTsynaptic membrane of the neuromuscular junction.
–Associated with other autoimmune diseases (RA, lupus)
TYPE 2 HYPERSENSITIVITY

Women 20-30, men >60

DESCENDING progressive weakness (according to the lecture)
Fatigable muscle weakness which may involve ocular, bulbar (of eyes, face, mouth, throat, and neck), respiratory and limb muscles (according to the BOOK)

Tx: Depends on subtype includes acetylcholinesterase inhibitors, corticosteroids & other immunosuppressives.

64
Q

What is Guillain Barre?
Causes?
Symptoms?
Treatment?
559-560

A

rare demyelinating disorder caused by humoral and cell mediated immunologic reaction directed at the peripheral nerves.
–there is a demyelinating subtype

Causes: usually within 4 weeks post respiratory or GI infection, associated with surgery, immunization, immune check point inhibitors, and infections (campylobacter, zika, COVID)

Symptoms: can vary widely, from tingling and weakness to ASCENDING flaccid paralysis progressing to complete quadriplegia with respiratory insufficiency and autonomic instability.

Treatment:
IVIG or plasma pheresis
—-Recovery is DESCENDING, takes weeks to 2 years.
20% will have residual weakness.

65
Q

What is Cerebral Palsy?
Causes?
Symptoms?
649

A

A permanent but not progressive disorder of movement, muscle tone, or posture caused by injury or abnormal development in the immature brain, before, during or after birth up to 1 yr.

Lecture says: occurs before 3 yrs, 70% before birth

Symptoms: spasticity, dystonia, ataxia, or a combination (mixed). Diplegia, hemiplegia, or tetraplegia.
MOST COMMON PYRAMIDAL/SPASTIC
—often have associated neurologic disorders such as seizures and intellectual impairment ranging from mild to severe.

66
Q

What are the 5 P’s of stroke?
Lecture

A

Parenchyma
Pipes
Perfusion
Penumbra
Prevent Complications

67
Q

TIA
Length
Symptoms
Risk
591-592 & lecture

A

episodes of neurologic dysfunction resulting from temporary arterial obstruction of brain blood flow, does not show evidence or acute infarct on imaging.
–Episodes last less than 24 hours (less than 60 minutes on the slides, about 15 minutes on google!!)

Symptoms: sudden severe HA, hemiparesis, numbness, sudden confusion, loss of balance, loss of vision, speech disturbances.

17% of people with TIA will have a stroke within 3 months

68
Q

Reversible ischemic neurologic deficit (RIND)
Lecture, AO & Google not in book

A

TIA but longer and no increased risk of stroke following.

Sudden deficits that reverse in more than or equal to 24 hrs (google says 7 days)

69
Q

Lacunar strokes
592 & Lecture

A

occlusion of a single, deep perforating artery that supplies a small penetrating subcortical vessel, causing ischemic lesions (0.5-15mm) or lacunes deep in the brain (thalamus or basal ganglia) but not the cortex
–accounts for 25% of ischemic strokes
–20% recurrence rate
–associated with cerebral small vessel disease and UNTREATED HTN

Symptoms: motor or sensory deficits due to location and small area of infarct, can also be silent

Lecture: deficits progress 24-36hrs, linked to vascular dementia

70
Q

Thrombotic Stroke
What is it?
592 & lecture

A

arterial obstruction caused by thrombus formation in arteries supplying brain or intracranial vessels, MOST OFTEN FROM ATHEROSCLEROSIS. (AND INFLAMMATION lecture)

Lecture: usually large vessel, ONLY type of stroke with slow progressive onset (AKA long term to make the atherosclerotic lesion?)

71
Q

Embolic Stroke
Most common vessel
592 & lecutre

A

involves fragments that break from thrombus formed outside the brain, usually the heart, aorta or common carotid artery. Can also be fat, air, tumor, bacterial lumps and foreign bodies.

MOST COMMON MCA

Deficit worst at onset

72
Q

What is a cryptogenic stroke?
591 & lecture

A

Ischemic Stroke with NO identifiable underlying cause

73
Q

Intracerebral Hemorrhage common location
Cause?
593

A

MOST COMMON LOCATION: deeper parts of the brain: basal ganglia, thalamus, pons and caudate nucleus.

Adjacent brain is deformed, compressed, and displaced causing ischemia, edema, increased intracranial pressure and necrosis. Expanding mass effect can cause brain stem herniation. Seepage or rupture into the ventricular system often occurs, and hydrocephalus can develop due to microscopic blood obstruction of the CSF outflow tracts.

MAX cerebral edema at 72 hrs and takes 14 days to subside.

Secondary injury from immune response, complement increases edema & RBC lysis, microglia/macrophages and leukocytes release inflammatory cytokines increasing inflammation. Oxidative stress increases cellular injury and death. Blood component breakdown products also promote secondary injury.

Cause: HTN!!

74
Q

Subdural Hematoma
Cause?
Shape?
574

A

bleeding between the dura mater and the arachnoid membrane covering the brain

CAUSED BY TEARING OF THE VEINS

MOST COMMON CAUSE OF TRAMATIC INTRACRANIAL MASS LESION (10-20%) rare cause anticoagulant therapy or vascular malformations.

Rapid onset (hours) for ACUTE, slower 24hrs to 2 wks for CHRONIC

CRESCENT SHAPED

75
Q

Epidural Hematoma
Cause?
Location?
Hallmark symptoms?
Shape?
574-575

A

bleeding between the dura mater and the skull.

Often a result of ARTERIAL BLEED
MOST COMMON SITE TEMPORAL FOSSA from
-MIDDLE meningeal artery
-ASSOCIATED WITH SKULL FX

Biconvex shape (shape of sun just before it sets on horizon/lense)

Sx: loss of consciousness at initial injury, a period of lucidity and then loss of consciousness again.

76
Q

Subarachnoid Hemorrhage
Cause?
Location?
Shape?
577-578

A

Bleeding into the subarachnoid space, between arachnoid and pia mater

ANEURYSM RUPTURE, but can also occur after TBI from shearing forces

MOST ARE MILD

Looks like starfish in middle of brain (lecture says blood in circle of willis cisterns and fissures but I think it looks like a starfish)

77
Q

Intracranial Hemorrhage
cause?
576 & lecture

A

Bleeding within brain tissue, may be single or multiple and are associated with contusions. Most are located in frontal and temporal lobes but may be in hemispheric deep white matter. ICH functions as an expanding mass increasing ICP, compressing brain tissues, and causing edema.

2-3% of head injuries

Can be caused by stroke to tumor as well

78
Q

Diffuse Axonal Injury
Cause?
Diagnosis?
578

A

involves widespread areas of the brain and occurs with all severities of brain injury. Results from mechanical effects of high level acceleration and deceleration injury such as whiplash or rotational forces that cause shearing and stretch of delicate axonal fibers and white matter tracts that project to or from the cerebral cortex.

Can only officially be diagnoses at autopsy with electron microscope. Often not visible on CT, but may be seen as diffuse punctate hemorrhages in areas where axons and small blood vessels are torn. (increased visibility 12hrs to days after injury)

Severity depends on force and location

KIDS HAVE NORMAL CTs BUT DON’T WAKE UP FOR DAYS/WEEKS/MONTHS

79
Q

Causes of secondary brain injury (6)
578 & AO

A
  1. Hypotension
  2. Hypoglycemia
  3. Hyponatremia
  4. Hypoxia
  5. Hypercarbia
  6. HYPERTHERMIA
80
Q

Complications of TBI
579

A
  1. Post concussion syndrome-> sports
    –Mild TBI.
    –Lasts weeks - mo
    –HA, dizziness, anxiety, fatigue, irritability, photophobia, depression
    –symptom management
  2. Chronic traumatic encephalopathy –> sports/repeated blast injury like soldiers, also called CTE (football)
    –progressive dementia
    –violent behavior, depression, suicide, memory loss
    –Diagnosis based on history and autopsy
  3. Post traumatic Seizure
    –10-20% of TBI
    –can be within days or up to 5 yrs or longer after
    –initial treatment with antiseizure medication at time of injury for one week. Only continue if seizure occurs.
81
Q

Spinal Cord Injury
Mechanism?
Grading (5)?
579-580

A

Initial mechanical trauma, and immediate tissue injury OR inadequate immobilization after injury. Flexion, extension, compression or rotation

Grades:
-Concussion: temporary disruption of cord function
-Cord contusion: bruising of neural tissue causing swelling and temporary loss of function
-Cord compression: pressure on cord causing ischemia- must be relieved
-Laceration: tear of tissues of cord, spectrum of injury severity
-Transection: severing of cord with permanent loss of function

82
Q

What are the vertebral level injury that causes:
Quadriplegia?
Paraplegia with arm control?
Paraplegia with trunk control?
Lecture

A

Quad: C6 and above

Para with arm: T6 and below

Para with trunk: L1 or below

83
Q

Febrile Seizures
Temp?
Simple vs complex?
Lecture

A

Fever with no other neurologic symptoms except for seizure, no CNS infection or other acute neurologic illness

Temp >38

Simple:
-6mo-5yrs
-Duration LESS than 15 minutes
-one in 24hrs
-generalized
-postictal with return to BASELINE

Complex:
-Any age
-Duration GREATER than 15 minutes
-Multiple seizures per 24hr period
-Generalized or focal
-Postictal may not fully return to baseline after multiple seizures

84
Q

What are the four phases of nociception?
503

A

-Transduction- receptor activation
-Transmission- nerve to spine to brain
-Perception- (has several requirements) coordination of meaning
-Modulation- facilitation or inhibition of pain signals

85
Q

What is Amyotrophic Lateral Sclerosis?
Cause?
Sufferers?
555 & AO

A

Lou Gehrig’s Disease

Progressive neurodegeneration of upper and lower motor neurons.

Amyotrophic- progressive muscle wasting (lower neurons)
Lateral Sclerosis- scarring of the spinal cord (upper neurons)

Cause unknown, some contributing genetic mutations 5-10% of cases, vast majority are “sporadic” with no identifiable genetic link.

More common in Caucasians, men, generally > 40yo, median on set 51-66yo.

86
Q

What is Spinal Shock?
Causes?
Trajectory?
581

A

temporary loss of spinal cord functions below the lesion. Spinal shock develops immediately after injury because of loss of continuous tonic discharge from the brain or brainstem and inhibition is central descending impulses.

Caused:
-cord hemorrhage
-edema
-anatomic transection

Trajectory:
normal activity below injury ceases
Transient drop in BP
bradycardia
poor venous circulation
loss of thermal control (lack of ability to vasoconstrict)

Progresses over hours, lasts 2-3 days
Takes weeks to months for return of reflexes

87
Q

Autonomic Dysreflexia
Patho?
Symptoms?
Causes?
582

A

Life threatening complication of spinal injury AT OR ABOVE T6

descending inhibition is blocked

Sx:
-paroxysmal HTN (up to 300!!)
-pounding HA
-blurred vision
-sweating above level of lesion
-flushing of skin
-nasal congestion
-nausea
-bradycardia

Cause:
MOST COMMON: bladder distention or constipation
-tight clothing or shoes
-pain below lesion

88
Q

Ionotropic Receptors
Which kinds of receptors
AO

A

directly controls the opening of ion channels. Critical for fast synaptic transmission

Rapid Response- immediate change in cellular excitability and activity.

Example:
Nicotinic acetylcholine receptors
Glutamate Receptors
GABA-A Receptors

89
Q

Metabotropic Receptors
Exampiof receptors
AO

A

upon binding with a neurotransmitter activates intracellular signaling pathways though second messengers

Slower response- slower but longer lasting effects
Modulate various cellular functions such as enzyme, ion channel activities and gene expression.

Example:
Muscarinic Acetylcholine Receptors
Dopamine Receptors
Serotonin Receptors

90
Q

Vasogenic Autoregulation
What is it
Under what circumstances does it fail
AO

A

Brain’s ability to maintain a relatively constant blood flow across a range of cerebral perfusion pressures ensuring adequate blood flow despite changes in systemic arterial pressures.

Only works when CPP is 50-150, outside this range becomes less effective increasing chances of ischemia or hyperemia

91
Q

What are the 4 ways the brain regulates cerebral blood flow
AO

A

Vasogenic Autoregulation: vasodilation/constriction

Metabolic Regulation: change blood flow based on its own metabolic activity

Respiratory Gas regulation: CO2 and O2 influence on vasodilation (high CO2=vasoconstriction, low O2=vasodilation to increase blood flow and O2 availability)

Neurogenic Regulation: nerves in blood vessels cause vasodilation/constriction based on signaling (sympathetic/parasympathetic)

92
Q

What are the 4 types of generalized seizures?
AO

A
  1. Tonic Clonic (grand Mal): stiffening and jerking
  2. Absence (Petit Mal): brief staring and unresponsiveness (seonds)
  3. Myoclonic: brief jerks or fast movements
  4. Atonic: sudden loss of muscle tone, head drop or falling

Advanced Patho Test 1 (20 decks)

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