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CCP Semester 2: The Path Of Shame > CCP 214 Neurological Emergencies 🧠 > Flashcards

CCP 214 Neurological Emergencies 🧠 Flashcards

1
Q

RASS +4

A

+4 Combative Overtly combative or violent; immediate danger to staff

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2
Q

RASS +3

A

+3 Very agitation Pulls on or removes tube(s) or catheter(s) or has aggressive behavior
 toward staff

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3
Q

RASS +2

A

+2 Agitated Frequent nonpurposeful movement or patient–ventilator dyssynchrony

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4
Q

RASS +1

A

Restless, Anxious, or apprehensive, but movements not aggressive or vigorous

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5
Q

RASS 0

A

0 Alert and calm

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6
Q

RASS -1

A

−1 Drowsy Not fully alert, but has sustained (more than 10 seconds) awakening,
 with eye contact, to voice

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7
Q

RASS -2

A

−2 Light sedation Briefly (less than 10 seconds) awakens with eye contact to voice

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8
Q

RASS -3

A

−3 Moderate sedation Any movement (but no eye contact) to voice

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9
Q

RASS -4

A

−4 Deep sedation No response to voice, but any movement to physical stimulation

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10
Q

RASS -5

A

−5 Unarousable No response to voice or physical stimulation

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11
Q

basal ganglia function

A
  1. fine-tune the voluntary movements
  2. fluidity of movement

Injury to the basal ganglia (such as in Parkinson’s) results in rigid movement

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12
Q

prefrontal cortex function

A
  1. Behaviour and executive function

2. purposeful mental action (reasoning)

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13
Q

occipital lobe function

A
  1. interpreting sensory information from the eyes (CN II)

2. primary visual cortex

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14
Q

temporal lobe function

A

short and long-term memory

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15
Q

parietal lobe function

A

integrating sensory information from various parts of the body

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16
Q

thalamus function

A

relays motor and sensory signals to the cerebral cortex

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17
Q

location of the brain’s respiratory centre

A

medulla oblongata and pons (brainstem)

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18
Q

location of the reticular activating system

A

The midbrain

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19
Q

Components of the brain stem exam

A
  1. Mode of ventilation
  2. Sedation level
  3. AVPU/Motor response/GCS
  4. Open eyes - is there movement? (CN III, midbrain)
  5. Pupil response to light (CN II, III, midbrain)
  6. Cough (CN X, medulla)
  7. Corneal (CN V, VII, pons)
  8. Gag (CN IX, X, medulla)
  9. Evaluate intrinsic respiratory drive (respiratory center, medulla)
  10. Tone (flaccid, rigid, spastic)
  11. Reflexes (Biceps C5, C6; Triceps C6, C7, C8; Brachioradialis C5, C6, C7; Patellar L2, L3, L4; Achilles tendon S1, S2; Plantar/Babinski; oculocephalic [Dolls Eyes] reflex CN VIII)
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20
Q

GCS M5 motor score correlates to what level of cortical dysfunction

A

minor dysfunction of the cerebral cortex

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21
Q

GCS M4 motor score correlates to what level of cortical dysfunction

A

Severe dysfunction of the cerebral cortex

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22
Q

GCS M3 motor score correlates to what level of cortical dysfunction

A

Severe damage above the brainstem (ie. thalamus)

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23
Q

GCS M2 motor score is correlated to what level of brain dysfunction

A

Dysfunction below the thalamus (brainstem involvement)

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24
Q

GCS M1 motor score is correlated to what level of brain dysfunction

A

Severe dysfunction of cerebral cortex with or without dysfunction of the brainstem

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25
Q

Broca’s area function

A

Expressive speech

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26
Q

Wernicke’s area function

A

Receptive speech interpretation and comprehension

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27
Q

Most effective interventions in reducing ICP

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Temp control (parenchyma volume and blood volume)
  2. PaCO2 control (intracranial blood volume)
  3. HOB 30 degrees (intracranial blood volume)
  4. Loosen tube ties/cervical collar/in-line neck positioning (intracranial blood volume)
  5. EVD (intracranial CSF volume)
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28
Q

Intracranial pressures (normal, abnormal, severe)

A
  1. Normal 5-15mmHg
  2. Abnormal > 20mmHg
  3. Severe > 40mmHg
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29
Q

Comprehensive neuro exam in an intubated patient

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Mode of ventilation
  2. Sedation level
  3. AVPU/Motor response/GCS
  4. Open eyes - is there movement? (CN III, midbrain)
  5. Pupil response to light (CN II, III, midbrain)
  6. Cough (CN X, medulla)
  7. Corneal reflex (CN V, VII, pons)
  8. Gag (CN IX, X, medulla)
  9. Evaluate intrinsic respiratory drive (respiratory center, medulla)
  10. Tone (flaccid, rigid, spastic)
  11. Reflexes (Biceps C5, C6; Triceps C6, C7, C8; Brachioradialis C5, C6, C7; Patellar L2, L3, L4; Achilles tendon S1, S2; Plantar/Babinski)
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30
Q

normal ICP values

A
  1. Normal adult range: 5-15 mmHg
  2. Intracranial hypertension: 20-30 mmHg
  3. Severe intracranial hypertension: >30 mmHg

Anything above 20mmHg is considered for treatment

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31
Q

functions of the cerebellum

A
  1. motor control
  2. Coordination of movement
  3. Balance/equilibrium
  4. regulation of Muscle tone
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32
Q

tentorium function

A

fold in the dura mater that separates the upper brain (supratentorium) from the lower brain (infatentorium) at the level of the cerebellar/occipital interface

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33
Q

cranial nerves originating from the pons

A
  1. trigeminal nerve (CN V)
  2. abducens nerve (CN VI)
  3. facial nerve (CN VII)
  4. vestibulocochlear (VIII)
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34
Q

cranial nerves originating from the medulla

A
  1. glossopharyngeal (CN IX)
  2. vagus (CN X)
  3. accessory (CN XI)
  4. hypoglossal (CN XII)
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35
Q

right sided cerebral blood flow pathway from LV to brain (anterior)

A

Aorta -> brachiocephalic -> right common carotid -> internal carotid -> circle of Willis -> MCA/AComm/ACA

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36
Q

right sided cerebral blood flow pathway from LV to brain (posterior)

A

Aorta -> brachiocephalic -> right vertebral artery -> basilar -> PCA/PComm

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37
Q

left sided cerebral blood flow pathway from LV to brain (anterior)

A

Aorta -> left common carotid -> left internal carotid -> circle of Willis -> MCA/AComm/ACA

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38
Q

left sided cerebral blood flow pathway from LV to brain (posterior)

A

Aorta -> left subclavian -> left vertebral -> basilar -> PCA/PComm

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39
Q

main vessels that arise from the Circle of Willis

A
  1. Middle cerebral arteries (MCA)
  2. Anterior cerebral arteries (ACA)
  3. Posterior cerebral arteries (PCA)
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40
Q

three types of cerebral aneurysms

A

fusiform, saccular, and berry

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41
Q

most common type of cerebral aneurysm

A
  1. Berry shaped aneurysm at a vessel bifurcation

2. The ACommA is the most common site for berry aneurysms and SAH

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42
Q

sudden onset dizziness, gaze palsy, nystagmus, N/V, ataxia, gait disturbance and incontinence

A

Cerebellar stroke (cerebellum regulates motor movements)

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43
Q

Potential clinical manifestations of basilar artery stroke (pons ischemia)

A
  1. Locked In Syndrome (total muscle paralysis)

2. Drop attacks

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44
Q

Potential clinical manifestation of PCA stroke (occipital ischemia)

A

vision impairment (blindness, hemianopsia)

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45
Q

“Classic” clinical findings in uncal herniation

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. ipsilateral dilated pupil that is unresponsive to light (CN III compression)
  2. altered mental status/coma
  3. contralateral hemiparesis
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46
Q

modified CN exam

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Open eyes, assess symmetry and size (midbrain CN II, III)
  2. Constriction x 2 pupils in response to light (midbrain CN II, III)
  3. Corneal reflex - eyes should blink (superior pons; middle pons CN V, VII)
  4. Doll’s eyes test if no c-spine concerns (inferior pons, CN VIII)
  5. Gag reflex (superior medulla, CN IX, X)
  6. Cough reflex (superior medulla, CN X)
  7. Respiratory drive (middle medulla)
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47
Q

key items not to miss on a CNS report

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Confounders such as sedation, hypothermia
  2. Brainstem reflexes, including any apneic periods
  3. GCS, especially motor exam
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48
Q

GCS - M6

A

Obeys

  • Obeys commands. Can look right/left, stick out tongue and give a thumbs up or wiggle fingers/toes
  • Squeezing the hands is a primitively response so avoid assessing it.
  • Indicates cortex is intact.
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49
Q

Score a GCS - M5

A

Localizes

  • Place arms at pt’s side and provide a pain stimulus (trap squeeze, supraorbital pressure). Pt’s contralateral arm must move across midline.
  • Indicates cortex is intact, but dysfunctional.
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50
Q

Score a GCS - M4

A

Withdraws

  • Place pt’s hands on abdo and provide constant fingernail stimuli. Pt’s hand must curl and pull away.
  • Indicates severe cortical dysfunction.
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51
Q

Score a GCS - M3

A

Abnormal Flexion

  • Place pt’s hands on abdomen and provide firm nail bed pressure. Pt’s hand must supinate and bicep will flex
  • Indicates dysfunction to thalami (internal capsule)
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52
Q

Score a GCS - M2

A

Abnormal Extension

  • Place pt’s hands on abdomen and apply constant fingernail pressure
  • Pt’s arms must fully extend with flexed triceps and hands rotated outwards
  • Feet will point down
  • Indicates dysfunction below the thalami (midbrain)
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53
Q

CNS reflex exam

A 
Biceps	C5, C6
Triceps	C6, C7, C8
Brachioradialis	C5, C6, C7
Patellar	L2, L3, L4
Achilles tendon	S1, S2

Grade on a scale of absent -> normal -> brisk

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54
Q

babinski reflex

A
  1. Stimulation of the lateral plantar aspect of the foot
  2. normally leads to plantar flexion of the toes (The toes curl down and inward)
  3. Babinski sign is positive when there is extension (dorsiflexion or upward movement) of the big toe +/- fanning of the other toes
  4. Positive Babinski is indicative of Upper Motor Neuron damage
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55
Q

dysarthria definition

A
  1. the muscles used for speech are weak (CN V, VII, IX, X, XII)
  2. Dysarthria causes slurred or slow speech that can be difficult to understand
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56
Q

dysphasia definition

A
  1. Dysphasia is a language disorder
  2. areas of the brain responsible for turning thoughts into spoken language are damaged and can’t function properly
  3. affects the ability to produce and understand spoken language
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57
Q

MOA for mannitol in controlling ICP

A
  1. Simple sugar which acts as an osmotic diuretic
  2. increased tonicity from the mannitol draws water out of the brain parenchyma and into the intravascular space via osmosis/diffusion
  3. water then travels with the mannitol to the kidneys where it gets excreted in the urine.

“Dries out the brain”

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58
Q

MOA for HTS in controlling ICP

A
  1. Dehydration of brain tissue by creation of an osmotic gradient
  2. Draws water from the parenchyma into the intravascular space
  3. Improved systemic volume improves cerebral perfusion via improvement in MAP in hypotensive poly trauma patients
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59
Q

How much fluid must you replace when using mannitol for reduction in ICP?

A

Measure urinary output and replace fluid (normal saline) at a 1:1 ratio

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60
Q

indications for anticonvulsant therapy in TBI

A
  1. Hx of seizure associated with the TBI
  2. Temporal lobe pathology
  3. Depressed/open skull fracture
  4. Penetrating trauma to the cranium
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61
Q

initial bundle of care for brain injury

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. MAP > 80 mmHg, SBP < 110-160 mmHg
  2. Normal temp (avoid hyperthermia)
  3. PaCO2 35-40 mmHg (target normal)
  4. PaO2 80-120 mmHg (target normal)
  5. Hgb > 90 g/L
  6. HOB 30°, loosen collars/ties
  7. Optimize platelets/INR
  8. Propofol/ketamine to RASS -4
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62
Q

WFNS (World Federal association of Neurosurgeons) score for SAH

A
  1. GCS 15, motor deficit absent
  2. GCS 13-14, motor deficit absent
  3. GCS 13-14, motor deficit present
  4. GCS 7-12 motor deficit present or absent
  5. GCS 3-6 motor deficit present or absent
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63
Q

DIMS mnemonic for differentiating seizures

A

Drugs
Infection
Metabolic and Endocrine
Structural (CNS)

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64
Q

clinical triad of symptoms in bacterial meningitis

A
  1. Fever
  2. Neuro symptoms (AMS/headache/photophobia/seizure)
  3. Nuchal rigidity
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65
Q

encephalitis definition

A
  1. inflammation of the brain, caused by infection or an allergic reaction
  2. most commonly viral
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66
Q

differentials for bilateral pinpoint pupils (miosis)

A
  1. Opioid overdose
  2. Pons bleed
  3. Cholinergic toxicity
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67
Q

Dosing for HTS in elevated ICP

A
  1. Elevated ICP: 3mL/kg (3% HTS)

2. Brain Herniation: 5mL/kg (3% HTS)

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68
Q

Dosing for mannitol in elevated ICP

A
  1. Elevated ICP: 0.25-0.5g/kg “maintenance dose”

2. Herniation: 1g/kg “herniation dose”

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69
Q

BP goal for an unsecured aneurysmal SAH

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

SBP < 140 mmHg

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70
Q

BP goals for ischemic CVA

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Pre lysis (r-TPA): SBP < 185 mmHg DBP <110 mmHg
  2. post lysis (r-TPA): SBP < 180 mmHg DBP <105 mmHg
  3. No lysis: SBP <220 mmHg DBP <120 mmHg
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71
Q

BP goals for acute hemorrhagic CVA

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

SBP < 140 mmHg

in the literature you’re gonna see a range from 140-160 for SBP, however for our purposes in BCEHS target <140. SBP of 160 is the upper limit of what is maximally acceptable

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72
Q

name the various herniation syndromes

A
  1. Subfalcine herniation (shifts under the falx cerebri)
  2. Transtentorial uncal herniation (anteromedial portion of temporal lobe (uncus) herniates medially into tentorial notch → compression on CN3)
  3. Central (trans-tentorial) herniation
  4. Cerebellar tonsillar herniation (herniation of the cerebellar tonsils through the foramen magnum → brainstem compression)
  5. Transcalvarial herniation (blowin’ out through a hole in the skull…)
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73
Q

ctyotoxic edema definition

A
  1. cerebral intracellular edema as a result of cells being unable to maintain ATP-dependent sodium/potassium (Na+/K+) membrane pumps which are responsible for high extracellular and low intracellular Na+ concentration
  2. Na+ accumulates within the cell, drawing with it chloride (Cl-) and water along an osmotic gradient
  3. CytE contributes to brain swelling with a resultant increase of intracranial pressure (ICP)
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74
Q

vasogenic edema definition

A
  1. cerebral extracellular edema which mainly affects the white matter via leakage of fluid from capillaries
  2. Vasogenic edema is characterized by extravasation and extracellular accumulation of fluid into the cerebral parenchyma caused by disruption of the BBB
  3. an insult to the blood vessels initiates the inflammatory cascade, vessel walls become more permeable and leak oncotic agents into interstitium
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75
Q

What is the danger in giving labetalol or hydralazine in TBI to control the BP?

A
  1. Hypertension often occurs transiently in TBI.
  2. If you give labetalol or hydralazine during an episode of transient compensatory HTN, those drugs can stay in the system long after the BP starts to naturally come down on its own. This will result in refractory hypotension (with decreased CPP)
  3. A better solution is to use escalating doses of propofol to augment your BP to achieve hemodynamic targets (fast on, fast off, easily titratable)
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76
Q

CCP treatment pathway for reducing ICP (Monroe-Kelly doctrine)

A
  1. Parenchyma (HTS, mannitol)
  2. Blood (PaCO2, BP, HOB 30 degrees, loosen collars/tube ties, OG, minimal PEEP, temperature control, sedation)
  3. CSF (EVD)
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77
Q

Cerebral Salt Wasting (CSW) definition

A
  1. endocrine condition characterized by hyponatremia and extracellular fluid depletion in response to acute disease in central nervous system (CNS), usually subarachnoid hemorrhage
  2. impaired sodium reabsorption → volume depletion, increased ADH release, hyponatremia d/t the associated water retention, and possibly increased neurologic injury
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78
Q

syndrome of inappropriate secretion of antidiuretic hormone (SIADH) definition

A
  1. disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (vasopressin)
  2. characterized by impaired water excretion → hyponatremia with hypervolemia or euvolemia (dilutional hyponatremia)
  3. levels of ADH are high even in the presence of decreased plasma osmolality and/or hyponatremia.
  4. Excess water absorption keeps the blood volume high or normal

restrict fluids

79
Q

Differentiating SIADH from CSW

A

1 . Both conditions are characterized by hyponatremia with elevated urine Na+, concentrated urine, and no edema.
2. in CSW the patient is hypovolemic versus in SIADH the patient is euvolemic to hypervolemic.

80
Q

Central diabetes insipidus (CDI) definition

A
  1. characterized by decreased release of ADH, resulting in a variable degree of polyuria
  2. due to a lack of the hormone vasopressin (antidiuretic hormone)
  3. This can be due to injury to the hypothalamus or pituitary gland or genetics
81
Q

What three arteries constitute the “posterior circulation”

A
  1. Basilar artery, vertebral artery, and posterior cerebral artery
82
Q

Bell’s Palsy definition

A
  1. paralysis of the facial nerve (CN VII) causing muscular weakness in one side of the face
83
Q

ACA stroke clinical presentation

think of the diagram of the homunculus. That diagram is fucking 💰

A
  1. primarily affect frontal lobe function
  2. Hemiparesis. Contralateral leg paresis more common than arm paresis
  3. bilateral leg weakness if both ACAs are involved
  4. Apraxia. disinhibition, diminished executive dysfunction
  5. Hemianesthesia
  6. Apathy
84
Q

TBI treatment plan checklist

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

A - Airway secured if needed, HOB 30 degrees, C-collar loosened, head in neutral alignment

B - PaCO2 - 35-45 (target normal), PaO2 - 80-120 (target normal), Peep <13 cmH2O

C - MAP > 80, SBP < 160 mmHg

D - Pupils, GCS, Motor exam completed and trended throughout transport.

E - Temp 36-37 (target normal, but prevent hyperthermia)

Labs - Na 140-150, Coag - INR < 1.5, PTT< 40, Platelets > 100, Fibrinogen > 1.0 Hemoglobin > 90

Herniation - Hypertonic, Mannitol, Hypervilation (PaCO 25-30)

85
Q

first, second, third line, 4th line options for status epilepticus (explain the seizure clock!! ⏰ ⏰ )

HIGH YIELD KNOWLEDGE BOMB 💣💣

A
  1. Benzodiazepines (5 min, 10 min) ⏰
  2. Anti-epileptics: Phenytoin, Keppra, valproic acid (15 min) ⏰
  3. Infusion therapy: Propofol, Midazolam, Ketamine (30 min) ⏰
  4. Rescue therapy: Deep barbiturate coma, Immunomodulatory therapy (anti-N-methyl-D-aspartate (NMDA) receptor encephalitis), Inhalational anesthetics (Isoflurane and desflurane) (45 min) ⏰

think of treating seizures like a 1 hour clock. You have your 4 phases of intervention staged in a q15 minute timeframe. Every 15 minutes you should be escalating to the next stage of shit, basically taking a liner, increasingly aggressive approach to getting on top of the seizures

86
Q

what patient population is phenytoin contraindicated in and why

A
  1. TCA OD due to sodium channel blockade
  2. Phenytoin has inherent sodium channel blocking properties
  3. Phenytoin will worsen the sodium channel blockade caused by the TCA Tox
87
Q

potential complications of SAH

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Re-bleeding
  2. Seizures
  3. Cardiogenic shock (takotsubo)
  4. Hydrocephalus
  5. Cerebral vasospasm
  6. Na+ imbalance (cerebral salt wasting)
88
Q

cerebrospinal fluid origins, and flow pathway

A
  1. created in the choroid plexus in the lateral ventricles
  2. flows through the interventricular foramina (foramen of Monroe) → 3rd ventricle
  3. From the 3rd ventricle, CSF flows → cerebral aqueduct to the 4th ventricle
  4. From the 4th ventricle CSF flows in the subarachnoid space around the cranium and → the spinal column
  5. It is re-absorbed in the archnoid villi of the superior sagittal vein
89
Q

clinical questions one must ask when evaluating a SCI patient

A
  1. Do they need intubation?

2. Are they in neurogenic shock?

90
Q

things to look for when deciding whether to intubate a spinal cord patient

A
  1. Nasal flaring
  2. sternocleidomastoid usage for breathing
  3. paralysis above the level of the biceps
  4. Normal PaCO2 with RR > 20
  5. Paradoxical breathing
91
Q

clinical significance of paralysis at or above level of the biceps in SCI

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. biceps are supplied by nerves at the level of C6, meaning C5 and above are intact
  2. The phrenic nerve (diaphragmatic innervation) originates from cervical spinal roots C3, C4 and C5
  3. This means that patients have full diaphgramatic control and likely do not need to be intubated
92
Q

drop attack definition

A

Drop attacks are sudden falls without loss of consciousness that are not precipitated by a specific stimulus, occur with abrupt onset and without warning, and are followed by a rapid return to baseline

93
Q

pathogenesis of “drop attack” in basilar artery stroke

A
  1. The vertebrobasilar arteries supply the cerebellum, medulla, midbrain, and occipital cortex.
  2. When the blood supply to these areas is compromised, it → ischemia of the reticular formation nuclei
  3. this results in Locked-in state (awake quadriplegia), Paralysis or weakness of all extremities, Horizontal gaze paresis, stupor, coma
94
Q

area of brain perfused by the basilar artery

A

midbrain/pons

95
Q

area of brain perfused by the PCA

A

occipital lobe

96
Q

Hgb target for a brain injured patient

A

90g/L

97
Q

testing brainstem reflexes in an intubated patient

A
  1. Pupil constriction reflex (II, III)
  2. Cornea reflex (V, VII)
  3. Cough (IX, X)
  4. Gag (IX, X)
  5. Respiratory effort (Respiratory centre)
98
Q

upper motor neuron (UMN) definition

this shit is super important for figuring out spinal pathways

A
  1. The impulses for movement are carried by nerves known as upper motor neurons (UMN)
  2. These motor nerves send messages between the cerebral cortex and the spine
  3. An UMN lesion is a lesion of the neural pathway above the anterior horn of the spinal cord or motor nuclei of the cranial nerves
  4. Damage to UMNs results in characteristic clinical manifestations colloquially termed “upper motor neuron signs” or “upper motor neuron syndrome.”
  5. UMN symptoms include muscle weakness, spasticity, hyperreflexia, and clonus. Damage to UMNs of the corticobulbar tract can manifest as dysphagia and dysarthria.
  6. Distinguishing upper motor neuron signs from lower motor neuron signs is essential in the neurological physical exam
99
Q

lower motor neuron definition

this shit is super important for figuring out spinal pathways

A
  1. A LMN is a multipolar neuron which connects the UMN to the skeletal muscle it innervates
  2. lower motor neurons directly innervate skeletal muscle and have cell bodies in the anterior horn of the spinal cord (ventral horn) and at cranial nerve nuclei
  3. Because lower motor neurons are cholinergic and directly innervate skeletal muscle, they can exist in both the central and peripheral nervous system (PNS)
  4. Lower motor neurons transmit impulses via spinal peripheral nerves or cranial nerves to skeletal muscles
  5. A LMN lesion is a lesion which affects nerve fibers traveling from the anterior horn of the spinal cord to the associated muscle(s)
100
Q

function of grey matter

A
  1. makes up the outer most layer of the brain (cortical)
  2. contains most of the brain’s nerve cells (neurons)
  3. enables individuals to control movement, memory, and emotions.
  4. processes information and releases new information through axon signalling (via white matter)
101
Q

function of white matter

A
  1. found in the deeper tissues of the brain (subcortical)
  2. contains nerve fibers (axons), which are extensions of nerve cells (neurons)
  3. many of these nerve fibers (axons) are myelinated. Myelin gives the white matter its colour
  4. White matter modulates the distribution of action potentials, acts as a relay and communication/coordination centre between different brain regions
102
Q

epidural hematoma CT findings

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. appears as a “lens” on CT scan. bi-convex, hyperdense, sharply demarcated.
  2. follows the curvature of the skull and protrudes into brain tissue as a convex mass
103
Q

lacunar stroke definition

A
  1. small subcortical lesions with a size of less than 15 mm in diameter
  2. caused by occlusion of a penetrating artery from a large cerebral artery, most commonly from the Circle of Willis
  3. most commonly found in basal ganglia, thalamus, pons, and subcortical white matter structures
104
Q

Inclusion criteria for tPA in stroke

A
  1. Clinical diagnosis of ischemic stroke causing neurologic deficit
  2. Onset of symptoms less than 4 ½ hours before beginning treatment
  3. Age over 18 years
105
Q

Contraindications for tPA in stroke

A
  1. ICH on CT
  2. Clinical presentation suggests SAH (thunderclap headache)
  3. Neurosurgery, head trauma, or stroke in past 3 months
  4. Uncontrolled HTN (>185 mmHg SBP or >110 mmHg DBP)
  5. History of ICH
  6. Known intracranial AVM, neoplasm, or aneurysm
  7. Active internal bleeding
  8. Suspected/confirmed endocarditis
  9. Known bleeding diathesis
  10. Abnormal blood glucose (<2.7 or >22.2 mmol/L)
106
Q

GCS correlation to severity of TBI

A
  1. 13-15 mild TBI
  2. 9-12 moderate TBI
  3. <8 severe TBI
107
Q

classic progression of CT findings in elevated ICP (aka stages of mass effect on CT-head)

A
  1. sulcal effacement (Effacement of the sulci adjacent to the lesion
  2. ventricular compression (partial or complete effacement of the adjacent ventricles)
  3. “Midline Shift” displacement of midline structures
  4. effacement of the contralateral ventricles and sulci
  5. herniation of structures (cerebral herniation)
108
Q

DO2 equation

A

DO2 = CO x (1.34 x Hgb x SaO2 + [PaO2 x 0.003])

109
Q

in the DO2 equation, how is “DO2” measured

A

mL (of oxygen) per minute

110
Q

in the DO2 equation, how is “CO” measured

A

L (of blood) per minute

111
Q

in the DO2 equation, what is “1.34” representative of

A

oxygen binding capacity of hemoglobin

1.34 mL of oxygen per gram of Hgb

112
Q

in the DO2 equation, how is “Hgb” measured

A

grams (of hemoglobin) per litre of blood

113
Q

in the DO2 equation, what is “SaO2” representative of

A

hemoglobin oxygen saturation

expressed as a fraction. for example, pulse oximetry saturations of “97%” would be represented as 0.97

114
Q

in the DO2 equation, what is “0.003 x PaO2” representative of

A

The amount of dissolved oxygen in the blood per mL

For every 1 mmHg of oxygen tension (PaO2), 0.003 mL of oxygen gas is dissolved in 100 mL of blood

115
Q

“classic case” clinical deterioration in EDH

A
  1. transient loss of consciousness
  2. “lucid interval” with recovery of consciousness, followed by deterioration over a period of hours
  3. associated with symptoms such as headache, vomiting, drowsiness, confusion, aphasia, seizures, and hemiparesis
116
Q

classic case CT findings in acute SDH

A
  1. 85% of SDH are unilateral
  2. extra-axial blood that spreads diffusely over the affected hemisphere
  3. crescent-shaped
  4. hyper-dense
117
Q

The four different vertebral column injury patterns leading to potential SCI

A
  1. Fracture of one or more of the bony elements
  2. Dislocation at one or more joints
  3. Tearing of ligament(s)
  4. Disruption and/or herniation of the intervertebral disc
118
Q

primary injury (TBI/SCI)

A
  1. immediate effects of trauma

2. includes forces of compression, contusion, and shear injury to the brain or spinal cord

119
Q

ASIA “A” SCI

A

Complete lack of motor and sensory function below the level of injury

120
Q

ASIA “B” SCI

A

Some sensation below the level of the injury

121
Q

ASIA “C” SCI

A

Some muscle movement is spared below the level of injury, but 50 percent of the muscles below the level of injury cannot move against gravity

122
Q

ASIA “D” SCI

A

Most (more than 50 percent) of the muscles that are spared below the level of injury are strong enough to move against gravity

123
Q

ASIA “E” SCI

A

SCI whereby all neurologic function has returned

Full recovery

124
Q

“classic case” CT-Head findings in SAH

A
  1. hyperdense material is seen filling the subarachnoid space
  2. Most commonly apparent around the circle of Willis
125
Q

“classic case” CT findings in IVH

A
  1. commonly occurs in the setting of intracerebral hemorrhage or subarachnoid hemorrhage
  2. Blood in the ventricles appears as hyperdense material
  3. blood is heavier than CSF, and thus tends to pool dependently
126
Q

“classic case” CT findings in cerebral contusion

A
  1. hyperdense foci in the frontal lobes
127
Q

“classic case” CT findings in DAI

A
  1. multiple focal lesions with a characteristic distribution
  2. typically located at the grey-white matter junction, in the corpus callosum
  3. in more severe cases present in the brainstem
128
Q

posterior spinal dorsal column (ascending sensory)

A

ascending pressure, vibration, discriminative touch, and proprioceptive sensation

  1. sensory neuron → dorsal column nuclei
  2. ipsilateral ascent in dorsal column → crosses over in medulla
  3. crosses over in medulla → contralateral ascent → synapse in thalamus (sensory relay center)
  4. thalamus → sensory cortex (postcentral gyrus)
129
Q

lateral spinal thalamic tract (ascending sensory)

A

ascending pain and temperature sensation

  1. sensory neuron → ipsilateral gray matter of spinal cord
  2. ipsilateral ascent in gray matter → crosses over 1-2 vertebrae above
  3. contralateral ascent in spinothalamic tract → synapse in thalamus (sensory relay center)
  4. thalamus → sensory cortex (post-central gyrus)
130
Q

lateral corticospinal tract (descending motor)

A

descending voluntary motor control

  1. UMN in motor cortex (pre-central gyrus) → ipsilateral descent through internal capsule
  2. crosses over at medulla → contralateral descent in lateral corticospinal tract
  3. synapse in anterior horn of spinal cord
  4. leaves anterior horn → synapses at neuromuscular junction (target muscle)
131
Q

spinal nerves present in the human body

how many pairs, what’s their distribution between the sections of spinal column

A

31 pairs

8 cervical
12 thoracic
5 lumbar
5 sacral
1 coccygeal
132
Q

neuro insults where the target SBP should be <140

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Subarachnoid bleed
  2. Epidural bleed
  3. Internal capsule bleed
  4. Ischemic stroke with hemorrhagic transformation

there are different references for this. generally for all intracranial bleeds you should target a max SBP of 160. there are some references that state you should have an absolute SBP of 140. Other references will say you can allow for a higher SBP of 160 for venous bleeds and should target a SBP of 140 for arterial bleeds/anything else.

133
Q

neuro insults where the target SBP should be <160 and MAP should be 80-90

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Undifferentiated TBI (SBP >110 <160, MAP >80)
  2. Subdural bleed (venous)
  3. Traumatic subarachnoid bleed
  4. DAI
  5. SCI (MAP 85-90 for cord perfusion)
  6. IVH
134
Q

pressors in neurogenic shock

A
  1. norepinephrine 1st line

2. Epinephrine if bradycardic

135
Q

Critical FVC for tubing GBS and MG

A

≤ 20mL/kg FVC

136
Q

Mechanisms to reduce “parenchyma” volume (Monroe-Kelly)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Osmotic therapy (mannitol/HTS)
  2. Sedation (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
  3. Temperature control (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
  4. Seizure control (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
137
Q

Mechanisms to reduce “CSF” volume (Monroe-Kelly)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. EVD (direct CSF drainage)
138
Q

Mechanisms to reduce “blood” volume (Monroe-Kelly)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Hyperventilation (decreased PaCO2 leads to cerebral vasoconstriction)
  2. Head in neutral alignment (cerebral venous drainage)
  3. HOB 30 degrees (cerebral venous drainage)
  4. Loosen C-Collar/ETT Ties (cerebral venous drainage)
  5. Decrease intra-abdominal pressure (cerebral venous drainage)
  6. PEEP <13cmH2O (cerebral venous drainage)
139
Q

the three hallmark features of central cord syndrome

A
  1. Arm paralysis > leg paralysis
  2. Bladder dysfunction
  3. Sensory loss below injury site
140
Q

clinical manifestations of ACA occlusion

A

Contralateral leg weakness/paralysis

141
Q

clinical manifestations of left MCA occlusion

A
  1. Right face
  2. Right arm
  3. speech
142
Q

clinical manifestations of right MCA occlusion

think of the image of the homunculus

A
  1. Left face
  2. Left arm
  3. speech
143
Q

possible clinical manifestations of basilar artery stroke

A
  1. Acute loss of consciousness
  2. normal pupils
  3. drop attack
  4. locked-in syndrome
  5. brainstem involvement (poor/absent respiratory effort)
144
Q

Aneurysmal Subarachnoid Hemorrhage treatment goals

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. securing the airway as needed
  2. blood pressure control (goal SBP <140 mm Hg)
  3. reversal of anticoagulation
  4. management of ICP
145
Q

Textbook clinical presentation for spontaneous SAH

A
  1. A thunderclap or instantly peaking headache (83% of patients)
  2. “worst headache of their life” (97% of patients)
  3. Nausea or vomiting (77% of patients)
  4. Neck stiffness or limited flexion (24%-35% of patients)
146
Q

Aneurysmal Subarachnoid Hemorrhage pathophysiology

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Aneurysmal SAH is a bleed into the subarachnoid space between the pia mater and the arachnoid mater
  2. The SA space is home to the CSF and is a true space, unlike the potential spaces that collect blood in subdural and epidural hemorrhages
  3. blood most commonly enters through the rupture of aneurysms, which typically develop at vessel bifurcation sites (d/t turbulent flow in these regions)
  4. Complications of aneurysmal SAH include intraventricular hemorrhage, hydrocephalus, intraparenchymal hemorrhage, and elevated ICP
147
Q

what are the characteristic findings for SAH on lumbar puncture

A
  1. RBCs: Intact RBCs will be seen early in the course of aneurysmal subarachnoid hemorrhage before lysis occurs in the CSF
  2. Xanthochromia: RBC lysis in the CSF results in a yellow discoloration
148
Q

Aneurysmal Subarachnoid Hemorrhage treatment pathway

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. IV/O2/Monitor
  2. Preliminary neuro exam
  3. secure the airway if req’d
  4. Art line/blood pressure control (goal SBP <140 mm Hg, labetalol, hydralazine, propofol, fentaNYL)
  5. reversal of anticoagulation (VitK/FFP/PCC/Plt/TXA)
  6. management of ICP (mannitol/HTS)
  7. prevent secondary brain injury (optimize venous drainage, treat pain/fever/electrolytes/glucose, Consider seizure prophylaxis, optimize BP/PaO2/pCO2)
149
Q

Intracerebral haemorrhage treatment goals

(deep parenchymal venous bleed)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. securing the airway as needed
  2. blood pressure control (goal SBP <160 mmHg, MAP 80-90)
  3. reversal of anticoagulation
  4. management of ICP
150
Q

Intracerebral haemorrhage pathophysiology

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. ICH is defined as bleeding within the brain tissue from parenchymal vessels, with the potential to extend into the ventricular system
  2. ICH is classified as primary (80%) or secondary (20%)
  3. Primary ICH is typically attributed to chronic HTN, secondary ICH can be caused by vascular malformation, tumor, coagulopathy, vasculitis, drug abuse, cerebral venous thrombosis, or anticoagulants
  4. In hypertensive hemorrhage, chronic stress on the endothelium results in lipohyalinosis → damage to small perforating arteries → arteries becoming brittle → to hemorrhage
  5. damage is commonly found in central locations such as the basal ganglia, thalamus, pons, midbrain, and cerebellum; may extend into the ventricular space
  6. ICH can be lobar or non-lobar, supratentorial or infratentorial
  7. 50% of intracerebral hemorrhages are deep, 35% are lobar, 10% are cerebellar, and 6% occur in the brainstem
151
Q

American Heart Association/American Stroke Association “door to needle” time for tPA in stroke

A
  1. door-to-needle time <60 min in 75% or more of patients

2. <45 min in 50% or more of treated patients

152
Q

ischemic stroke pathophysiology

A
  1. focal area of neuronal hypoperfusion → oligemia, impaired oxygen and glucose metabolism, and eventual ischemia and infarction
  2. Large vessel disease is a product of HTN causing endothelial damage and atherosclerotic plaque formation. Ulcerated plaques propagate, causing progressive stenosis, obstruction or embolization.
  3. Small vessel disease is caused by lipohyaline arteriolosclerosis, usually of branching/penetrating arteries that are less elastic and more susceptible to collagen deposition, which progresses with age
153
Q

most common TIA and stroke mimics

A
  1. partial seizures (44%)
  2. complicated migraine (24%)
  3. radiculopathy
  4. hypoglycemia
  5. metabolic derangement
  6. infection
  7. psychogenic causes
154
Q

key components of a comprehensive neurological exam

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Mental status and higher cortical function
  2. Cranial nerves
  3. Sensory function
  4. Motor function
  5. Gait and coordination
  6. Reflexes
155
Q

American Heart Association/American Stroke Association definition of TIA

A

transient loss of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction

156
Q

cerebral perfusion pressure required to maintain cerebral auto regulation

A
  1. 50-70 mmHg

mean average CPP = 60mmHg.

CPP = MAP - ICP

157
Q

Blood pressure targets in acute CVA patients (ischemic stroke)

A
  1. Hypotension should be avoided and corrected when present to maintain optimal CPP
  2. Unless the patient is a candidate for IV rtPA, permissive HTN should be allowed up to 220/120 mmHg
  3. Patients receiving rtPA should have a blood pressure <185/110 mmHg before rtPA administration
  4. Post rtPA target BP <180/105
  5. If the patient develops “hemorrhagic transformation” drop your BP targets to SBP <160/MAP >80
158
Q

Atlanto-Occipital Dissociation

A

Subluxation or dislocation of the atlanto-occipital joint. Typically caused by severe extension plus distraction or hyperflexion

unstable injury. bad prognosis

159
Q

Jefferson burst fracture (C1 Fracture of the Atlas)

A

Axial load drives the occipital condyles into C1 → C1 fracture

160
Q

Hangman fracture (C2: Fractures of the Axis)

A
  1. Traumatic Spondylolisthesis
  2. Severe hyperextension causes fracture of the bilateral C2 pedicles, allowing the body of C2 to slide forward relative to C3
  3. Classically thought of as occurring in judicial hangings (not suicidal)
  4. More commonly observed in motor vehicle collisions and diving accidents
  5. Unstable injury
  6. External stabilization is typically sufficient.
161
Q

C3 - C7 Burst Fracture

A
  1. axial loading → comminuted fracture of the vertebral body
  2. Can have retropulsion of fragments into the spinal canal
  3. Can be unstable, depending on the presence of neurologic deficits and/or spinal canal compromise and the degree of vertebral damage
  4. Unstable injuries require surgical decompression
162
Q

C3-C7 Wedge/Compression Fracture

A
  1. hyperflexion → compression of the anterior aspects of vertebral bodies against one another
  2. unstable if >50% loss of vertebral height or if there are multiple contiguous wedge fractures
163
Q

C3-C7 Flexion Teardrop Fracture

A

hyperflexion → collision of vertebral bodies

Unstable injury (often anterior cord syndrome)

164
Q

C3-C7 Extension Teardrop Fracture

A

Sudden hyperextension → avulsion fracture of anteroinferior aspect of vertebral body.

common mechanism is a diving accident

Unstable injury associated with severe spinal cord injuries

165
Q

Anterior cord syndrome

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Characterized by damage to the anterior two-thirds of the spinal cord
  2. causes complete loss of motor function and sensation of pain and temperature below the injury
  3. Posterior column sensations of vibration, proprioception, and light touch are preserved
  4. typical mechanisms include flexion injuries, retropulsion of fracture fragments, or occlusion of the anterior spinal artery
166
Q

Brown-Sequard syndrome

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Lateral hemisection of the spinal cord
  2. typically from a penetrating injury
  3. Loss of ipsilateral motor function, light touch, proprioception.
  4. Loss of contralateral pain and temperature sensation.
167
Q

Central cord syndrome

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. bilateral upper extremity motor weakness with relative sparing of the lower extremities
  2. Distal muscles are typically affected more than proximal
  3. Makes up almost 10% of adult SCI and classically occurs during a hyperextension injury
  4. May occur without fracture, especially in older patients or those with spinal stenosis
  5. Hyperextension of the cervical spine causes buckling of the ligamentum flavum, which → localized injury within the center of the spinal cord
168
Q

Neurogenic shock

A
  1. characterized by hypotension and bradycardia
  2. Injuries above T6 can result in sympathetic disruption and neurogenic shock
  3. Bradycardia is more common in higher cervical injuries
  4. The hypotension of neurogenic shock is a distributive process (dry, warm/flushed skin with strong peripheral pulses)
  5. Neurogenic shock is a diagnosis of exclusion.
  6. Bradycardia can be seen in trauma patients for numerous reasons, including extremes of age, medication use (like beta blockers)
  7. Norepinephrine should be the primary agent used in neurogenic shock
  8. Epinephrine for profound bradycardia and hypotension
169
Q

Autonomic dysreflexia

A
  1. potentially life-threatening condition observed in patients with injury above the level of splanchnic sympathetic outflow (T6)
  2. A stimulus below the level of injury triggers uninhibited sympathetic output → hypertension and the classic symptoms of diaphoresis and flushing above the level of injury, nasal congestion, blurred vision, anxiety, bradycardia, and severe headache with the risk of intracranial hemorrhage or other hypertensive end-organ damage
  3. the most common trigger is bladder distension, followed by bowel distension or fecal impaction
170
Q

relationship between serum Na+ and brain injured states

A
  1. Sodium is a major determinant of fluid balance homeostasis
  2. hyponatremia is aggressively avoided in brain injured states
  3. low serum sodium leads to a hypoosmolar state that results in a shift out of the vascular compartment and into the cerebral parenchyma, leading to cerebral edema
  4. target sodium 140-150 (high-normal)
171
Q

MCA stroke clinical presentation

A
  1. MOTOR CORTEX - contralateral paralysis of upper arm + face
  2. SENSORY CORTEX - contralateral loss of sensation of upper arm + face
  3. SPEECH - aphasia if in dominant hemisphere (usually left)
  4. VISUAL - hemineglect if in non-dominant hemisphere (usually right)
172
Q

ACA stroke clinical presentation

A
  1. MOTOR CORTEX - contralateral paralysis of lower leg
  2. SENSORY CORTEX - contralateral loss of sensation of lower leg
  3. BALANCE/COORDINATION - apraxia
  4. MOOD - apathy
173
Q

Upper motor neuron signs

A
  1. hyperreflexia
  2. Babinski sign
  3. Hoffman reflex present
  4. clonus
  5. spasticity
174
Q

Internal capsule (lenticulo-striate artery) stroke clinical presentation

A
  1. MOTOR CORTEX - contralateral hemiparesis that affects the face, arm, and leg in equal parts

common site of lacunar infarcts

175
Q

PCA stroke clinical presentation

A
  1. VISUAL CORTEX - contralateral hemianopia (you knock out the 1/2 field of vision contralateral to the side of the infarct)
176
Q

Basilar artery stroke clinical presentation

A
  1. BRAINSTEM (pons/medulla/lower midbrain) - preserved consciousness but loss of voluntary facial/mouth/tongue movement. Loss of brainstem function with “locked in syndrome”

these guys are super tenuous. don’t sedate these guys. keep them on no sedation on pressure support ventilation. The reason why is that your brainstem exam (spontaneous respiratory effort) is your only component of the neuro exam you can trend because they are otherwise 100% flaccid

177
Q

most common vessel responsible for epidural bleed

A

middle meningeal artery (MMA)

178
Q

goal BP/MAP in multi system trauma with comorbid TBI

A
  1. MAP >80mmHg

2. SBP >110 <160

179
Q

goal BP/MAP for ICH/intraparenchymal bleeds (deep brain parenchyma)

A
  1. ICH bleeds are normally venous = low pressure

2. Target SBP <160, follow normal TBI care plan (MAP >80, optimize venous drainage etc.)

180
Q

cerebral perfusion pressure normal range

A

Normal CPP lies between 60 and 80 mm Hg

181
Q

MOA for phenytoin

A
  1. non-specific voltage-gated sodium channel blocker
  2. prevents seizures by inhibiting the positive feedback loop that results in neuronal propagation of high frequency action potentials
182
Q

MAP goal in an isolated spinal cord injury

A

MAP > 85

“drive that MAP to perfuse the cord!”

183
Q

Define and describe spinal shock aka “shocked spine”

note: DIFFERENT FROM NEUROGENIC SHOCK

A

a temporary stunning of the spinal cord → a transient flaccid paralysis and anesthesia distal to the spinal cord injury that usually lasts days to weeks before spontaneous improvement

184
Q

differentiate + describe the difference between neurogenic shock and spinal shock

💵💵💵💵 MONEY SLIDE 💵💵💵💵

💣💣💣KNOWLEDGE BOMB 💣💣💣

A

SPINAL SHOCK aka “SHOCKED SPINE”: a temporary stunning of the spinal cord → a transient flaccid paralysis and anesthesia distal to the spinal cord injury that usually lasts days to weeks before spontaneous improvement

NEUROGENIC SHOCK: form of distributive shock classically characterized by hypotension and bradycardia. Injuries above T6 → sympathetic disruption → a distributive process, resulting in dry, warm/flushed skin with good peripheral pulses

185
Q

Spinothalamic tract (define and describe)

A
  1. Ascending pathways responsible for communicating sensations of light touch, pain, and temperature to the brain.
  2. Has anterior and lateral components.
186
Q

Posterior spinal columns AKA posterior grey column (define and describe)

A
  1. Ascending pathways responsible for communicating sensations of deep touch, proprioception, and vibration to the brain.
  2. Ventrally located.
187
Q

Corticospinal tract (define and describe)

A
  1. major descending motor pathway,
  2. contains anterior and lateral components (lateral more prominent)
  3. Directs motor movement
188
Q

Anterior cord syndrome – (define and describe)

A
  1. damage to the anterior 2/3’s of the spinal cord → complete loss of motor function and sensation of pain and temperature below the injury.
  2. Posterior column sensations of vibration, proprioception, and light touch = intact
  3. Typical MOI = flexion injuries, retropulsion of fracture fragments, or occlusion of the ASA

shitty prognosis

189
Q

Brown-Sequard syndrome (define and describe)

A
  1. Lateral hemisection of the spinal cord → Loss of IPsilateral motor function, light touch, proprioception + Loss of CONTRAlateral pain and temperature sensation.
  2. typically from penetrating MOI
190
Q

Central cord syndrome – (define and describe)

A
  1. bilateral upper extremity motor weakness with relative sparing of the lower extremities
  2. Distal muscles typically affected more than proximal.
  3. classically occurs during a hyperextension injury. Hyperextension of the cervical spine → buckling of the ligamentum flavum → localized injury within the center of the spinal cord
  4. May occur without fracture, especially in older patients or those with spinal stenosis

good prognosis

191
Q

hallmark physical exam findings in Guillain-Barré syndrome (GBS)

A

Ascending paralysis with concordant loss or weakness of deep tendon reflexes.

192
Q

Myasthenic crisis (define and describe)

A

a complication of myasthenia gravis characterized by worsening of muscle weakness, resulting in respiratory failure that requires intubation and mechanical ventilation.

193
Q

Myelitis (define)

A

Heterogenous group of disorders that cause inflammation of the spinal cord

CCP Semester 2: The Path Of Shame (20 decks)

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