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B&B Part 1 > B&B Week 4 > Flashcards

B&B Week 4 Flashcards

1
Q

define consciousness

A

a state of awareness of self and environment, and awareness of the relationship between self and environment

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2
Q

what are the 3 neural correlates of consciousness?

A
  1. STATE of consciousness
  2. LEVEL of consciousness
  3. CONTENT of consciousness
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3
Q

what is responsible for “state” of consciousness?

A

refers to responsiveness to stimuli (i.e verbal, pain, etc)

multiple regions of the THALAMUS… thalamus and thalamic signalling–> the “gatekeeper” to the cortex

synchronized signalling between thalamus and cortex generates the STATE of consciousness

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4
Q

what is responsible for “level” of consciousness?

A

alertness–> drowsiness–> coma… its a continuum

diffuse BRAINSTEM structures–> projections from the brainstem reticular formation (RF) to the thalamus and cortex

projections between thalamus and cortex

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5
Q

what is responsible for “content” of consciousness?

A

sensations, emotions, memories and feelings that occur in our inner world –> perception, emotion, meaning, memories…

main player is the cortex which is accessed thru the thalamus …widespread regions of the CEREBRAL CORTEX

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6
Q

what are the 4 main neural players in consciousness?

A
  1. brainstem reticular formation
  2. thalamus
  3. thalamic reticular nucleus (TRN)
  4. cortex
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7
Q

where is the brainstem RF located?

A

in the tegmentum of the brainstem extending into the spinal cord

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8
Q

what are the 3 functional components of the brainstem RF?

A
  1. lateral zone–> processes afferent, sensory information
  2. medial zone–> processes efferent, motor information
  3. the sum of neurotransmitter systems that project to widespread areas of the CNS
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9
Q

what does the lateral zone of the brainstem RF do?

A

processes afferent, sensory information

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10
Q

what does the medial zone of the brainstem RF do?

A

processes efferent, motor information

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11
Q

what do the the sum of neurotransmitter systems that project to widespread areas of the CNS from the brainstem RF do?

A

influence the level of consciousness, wakefulness and sleep, as well as play a role in pain processing, motivation, emotion, reward, and addiction

together, the projections from the RF that ascend to the thalamus and cortex and play a role in modulation of consciousness are often referred to as the ascending reticular activating system (ARAS)

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12
Q

what is the ARAS? what is involved in it?

A

together, the projections from the RF that ascend to the thalamus and cortex and play a role in modulation of consciousness are often referred to as the ascending reticular activating system (ARAS)

  1. dopamine–> substantia nigra and ventral tegmental area
  2. noradrenaline–> locus ceruleus–> projects to thalamus and forebrain
  3. serotonin–> raphe nuclei–> projects to thalamus, cortex, basal ganglia, brainstem
  4. ACh–> tegmentum of pons–> projects to thalamus and cortex to strengthen output from thalamus to cortex
  5. histamine–> tegmentum of midbrain–> projects to thalamus and cortex for general arousal and alertness
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13
Q

what is the role of the thalamus in consciousness?

A

connects cortical areas with each other, integrating, modulating and gating the flow of info from one part of the cortex to the other

because it regulated information that will ultimately reach the cortex, it is called the “Gatekeeper” to the cortex

bidirectional communication between the cortex and nuclei of the thalamus provides an additional layer of information processing

contains specific inputs (drivers) and regulatory inputs (modulators)–> drivers contain info that must be forwarded to the cortex and modulators regulate whether or not it is forwarded

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14
Q

what is the role of the thalamic reticular formation (TRN) in consciousness?

A

the TRN is a sheet of neurons surrounding the thalamus

all neurons of the TRN are GABAergic and send their inhibitory projections into the thalamus, thereby negatively modulating the excitatory projections between the thalamus and the cortex (“gatekeeper of the gatekeeper”)

for conscious awareness, the connections between the TRN and the thalamus, and between the cortex and the TRN must be SYNCHRONIZED

consciousness means that the external and the internal experiences of an event are one, or are synchronized in time and space –> through this synchronization, the TRN creates consciousness or awareness of incoming sensory stimuli and cognitive processes

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15
Q

when neurotransmitter do the neurons in the TRN use?

A

GABA–> are all inhibitory

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16
Q

what is the role of the cortex in consciousness?

A

the cortex computes the CONTENT of consciousness where the thalamus DISPLAYS, and thus experiences, the results of those computations

different areas involved including the prefrontal (attention) and parietal areas (social) or cortex

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17
Q

what is the basic concept underlying unconsciousness (neurally)?

A

regardless of the cause, the basic concept underlying unconsciousness is that at least one of two areas must be damaged, either:
1. ascending reticular activating system (ARAS)
or
2. bilateral cerebral hemispheres or thalamo-cortical projections

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18
Q

what is a mnemonic for remembering the structural causes of unconsciousness?

A

TIPS

trauma/tumour/temperature
infection
psychogenic
subdural hematoma/subarachnoid hemorrhage/stroke/seizure

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19
Q

what are the structural causes of unconsciousness?

A

TIPS

trauma/tumour/temperature
infection
psychogenic
subdural hematoma/subarachnoid hemorrhage/stroke/seizure

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20
Q

how does trauma lead to unconsciousness?

A

head injury leads to loss of consciousness via several mechanisms

primary injury, produced at the moment of impact, includes COUP CONTUSION (at site of impact) and CONTRE-COUP CONTUSION (at the side opposite to that of impact) of the brain, which can lead to SUBDURAL or EPIDURAL hemorrhage

another mechanism of primary injury in head trauma is DIFFUSE AXONAL INJURY from the compressive, tensile and shear forces exerted on the brain–> shear injury predominates in white matter fibre tracts, disrupting a vast area of both cerebral hemispheres

secondary insults resulting from head trauma include intracranial hemorrhage (brain parenchyma, subdural or epidural space), raised ICP, hypoxia/ischemia, sepsis (usually due to lung or urinary infection that becomes systematic) and electrolyte disorders (SIADH, diabetes insipidus)

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21
Q

what happens when you have a lesion like a tumour, subdural hematoma, subarachnoid hemorrhage or stroke (unilateral, supratentorial, space occupying lesions)?

A

these types of lesions result in increased ICP, which leads to herniation syndromes

following munroe-kellie doctrine, the increased ICP leads to medial or UNCAL herniation through the tentorial notch beside the midbrain, distorting the midbrain ARAS, leading to decreased alertness

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22
Q

list the 5 mechanisms by which tumours can cause impaired consciousness

A
  1. mass effect from the tumour, edema or hemorrhage
  2. strategic location
  3. meningeal spread
  4. complication of therapy
  5. seizures
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23
Q

what are the most important factors concerning mass effects of tumours on consciousness?

A

speed of tumour growth and location

causes of rapid evolution of mass effect include:

  • hemorrhage into a tumour
  • cerebral edema
  • necrosis of the tumour with swelling or rapid growth

tumours within or near centers for alterness (rostral brainstem, thalamus or, less likely, BOTH frontal lobes) can cause compression or distortion of these centers leading to decreased consciousness

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24
Q

how does tumour spread to meninges cause impaired consciousness?

A

can lead to obstruction of CSF circulation, hydrocephalus, and raised ICP

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25
Q

what might cause a seizure in a brain cancer patient?

A

may be due to brain or meningeal mets, chemo-related metabolic disturbance, infections, or, less commonly, a direct effect of a drug, all of which can lead to decreased consciousness

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26
Q

how does temperature affect consciousness?

A

hyperthermia–> in pyrexia (rectal temp greater than 41 degrees celcius), neurologic function is impaired due to several mechanisms

hypothermia–> in severe hypothermia (less than 25 degrees celcius) there is a LOSS OF CEREBROVASCULAR AUTOREGULATION and thus cerebral blood flow declines… furthermore, the combined effects of platelet dysfunction, increased fibrinolytic activity and release of a heparin-like substance produces a DIC-like syndrome

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27
Q

what are the mechanisms by which pyrexia (hyperthermia) impairs neurologic function?

A
  1. IL-1 and other cytokines have a direct effect on the CNS
  2. brain concentration of EXTRACELLULAR GLUTAMATE is directly related to temperature–excessive amounts can lead to an encephalopathy and seizures
  3. systemic abnormalities from pyrexia (hypoglycemia, hypophosphatemia, electrolyte disturbances, uremia, other end organ damage) contribute to encephalopathy
  4. hemorrhages can occur in various organs (including the brain) at high temps due to endothelial damage and disseminated intravascular coagulation (DIC)–> common areas of brain hemorrhage include the cerebellar cortex, cerebral cortex, thalamus, striatum
  5. it has been proposed that activation of NMDA receptors plays a role in hyperthermia
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28
Q

what is pyrexia?

A

rectal temp greater than 41 degrees celcius

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29
Q

how does infection cause unconsciousness?

A

the mechanisms behind coma in CNS infections are complex and include disturbances of the microvasculature and larger cerebral arteries, and result in altered cerebral metabolism, altered cerebral blood flow, cerebral edema, increased ICP, focal cerebral lesions (including mass lesions with resulting tentorial or foramen magnum herniation) and hydrocephalus

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30
Q

how do psychogenic mechanisms cause unconsciousness?

A

unresponsiveness is a diagnosis of exclusion

the neuro exam shows REACTIVE PUPILS and NO REFLEX POSTURING to PAIN (i.e no decerebrate or decorticate posturing)

eyes remain in midgaze during the oculocephalic reflex, hence there is an ABSENT DOLL’S EYE response

ice water caloric testing will either INDUCE NYSTAGMUS or ROUSE the patient because of the discomfort produced

the EEG finding in psychogenic unresponsiveness reflects that of NORMAL WAKEFULNESS

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31
Q

what is decorticate posturing?

A

Decorticate posture is an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight. The arms are bent in toward the body and the wrists and fingers are bent and held on the chest.

This type of posturing is a sign of severe damage in the brain. People who have this condition should get medical attention right away.

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32
Q

what is decerebrate posture?

A

Decerebrate posture is an abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward. The muscles are tightened and held rigidly. This type of posturing usually means there has been severe damage to the brain.

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33
Q

what is the oculocephalic reflex and the doll’s eye response?

A

oculocephalic reflex:
ensure the C-spine is cleared.
the patient’s eyes are held open.
the head is briskly turned from side to side with the head held briefly at the end of each turn.
a positive response occurs when the eyes rotate to the opposite side to the direction of head rotation, thus indicating that the brainstem (CN3,6,8) is intact.

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34
Q

how does a subdural hematoma cause unconsciousness?

A

subdural hematomas are more common that epidural hematomas, occurring in approx 30% of severe head injuries

result most frequently from tearing of a bridging vein between the cerebral cortex and a draining venous sinus

with subdural hematomas, the force of impact is often transmitted to the brain itself

a subdural hematoma will appear on a CT scan as a crescent shaped blood collection between the brain and the dura

there is frequently an adjacent parenchymal contusion, and if large it may cause a midline shift, leading to uncal herniation and altered consciousness

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35
Q

how does subarachnoid hemorrhage lead to unconsciousness?

A

saccular and berry aneurysms of intracranial arteries lie unsupported in the subarachnoid space–> rupture of these thin walled vessels is the primary cause of subarachnoid hemorrhage

although the most common presenting symptom is an intense headache, accumulation of blood in the cranium can lead to a mass effect, leading to uncal herniation and altered consciousness

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36
Q

how does stroke cause unconsciousness?

A

the two classes of strokes are hemorrhagic (cause unconsciousness by similar mechanism to subarachnoid hemorrhage) and ischemic

ischemic strokes from thrombus or embolus blocking the vessel lumen account for 80% of strokes

ischemic strokes can cause altered consciousness if the involved vessel supplies the MIDBRAIN (i.e the vertebral-basilar system–> posterior cerebral artery)

infarcts of the internal carotid system are LESS likely unless there are bilateral infarcts of the anterior cerebral arteries

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37
Q

which are more common, ischemic or hemorrhagic stroke?

A

ischemic (80%)

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38
Q

how do seizures cause unconsciousness?

A

in generalized tonic-clonic seizures, the entire CNS is dominated by cycles of excitation and inhibition, thus all measures of consciousness are lost and a temporary coma results

in complex partial seizures, impaired consciousness usually reflects the spread of the seizure discharge throughout the LIMBIC system bilaterally

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39
Q

what is a mnemonic for remembering the metabolic causes of unconsciousness? what are the causes?

A

AEIOU

Alcohol
electrolyte imbalance
infection/insulin
oxygen/opiates/other drugs
uremia
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40
Q

how does alcohol cause unconsciousness?

A

alcohol is a CNS depressant that is through to potentiate the receptor function of the inhibitory amino acid GABA and inhibit the receptor function of the excitatory animo acid NMDA

alcohol also increases membrane fluidity and permeability, thus reducing the speed of synapses

it also acts on noradrenergic, dopaminergic, serotoninergic and opioid pathways

with high blood alcohol levels, stupor (0.4 blood alcohol) and coma (0.5 blood alcohol) can occur in acute alcohol intoxication

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41
Q

how does electrolyte imbalance cause unconsciousness?

A

confusion and coma can result from anything that causes HYPONATREMIA, or HYPERCALCEMIA

the (reversible) toxic effects of these abnormalities on the brain are not understood but may, in different cases, impair energy supplies, change ion fluxes across neural membranes, and cause neurotransmitter abnormalities

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42
Q

how can insulin (hypoglycemia) cause unconsciousness?

A

HYPOGLYCEMIA can cause neuronal death (and severe hypoglycemic reactions are commonly accompanied by seizures or by status epilepticus that can also contribute to cell death)

in hypoglycemic coma, extracellular CALCIUM concentration FALLS profoundly and intracellular calcium rises before energy stores are depleted

neuronal death is presumed to be calcium-mediated, with activation of free radicals and release of other autodestructive enzymes

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43
Q

how does hyperglycemia affect consciousness?

A

hyperglycemia can also cause decreased alertness

impairment of consciousness correlates with the degree and rapidity of the hyperosmolality, mainly due to cellular dehydration and volume loss

acetoacetate (not beta-hydroxybutarate) in high concentrations in diabetic ketoacidosis produces impaired consciousness and decreased cerebral oxygen use

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44
Q

how does hypoxia cause unconsciousness?

A

hypoxia results in cell death by a complex mechanism involving several components

hypoxia is most often accompanied by ischemia, which leads to cell death and glutamate release that stimulates NMDA receptors, thus stimulating calcium entry into cells

this increased intracellular calcium activates intracellular enzymes and genes, leading to cell damage and eventual cell death

upon dying, it releases its contents and perpetuates the cycle

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45
Q

how do opiates cause unconsciousness?

A

there are many types of opioid receptors to which these drugs can bind (Mu, kappa, delta, sigma and epsilon)

kappa receptors’ actions include analgesia, sedation, respiratory depression and miosis (since there is a high density of opioid receptors in the brain stem nuclei)

**almost any drug in sufficient quantity can cause coma

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46
Q

how does uremia cause unconsciousness?

A

unlike ammonia, urea itself does not produce CNS toxicity

therefore, a multifactorial cause for coma has been proposed including an increased permeability of the BBB to toxic substances such as organic acids and an increase in brain calcium or CSF phosphate content

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47
Q

what makes up intracranial volume?

A

80% brain

10% CSF

10% blood

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48
Q

what is the munroe-kelli doctrine?

A

(Vk is constant)

Vk equals Vbrain + Vcsf + Vblood

therefore, any ADDED volume within the skull displaces the other 3 normal constituents–> increase in pressure within the confined rigid skull (normally

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49
Q

what procedure is contraindicated in elevated ICP states?

A

lumbar puncture (risk of herniation)

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50
Q

how do you monitor ICP?

A 
predominant methods are:
extraventricular drains (ventriculostomy)
fibre-optic pressure transducers

ventriculostomy relieves elevated ICP and hydrocephalus when CSF flow is obstructed

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51
Q

what is the major pathological result of closed head injuries?

A

increased ICP

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52
Q

what are the cellular effects of increased ICP?

A

mechanical compression on neurons, glia, and cerebral blood vessels

this causes neuronal dysfunction and eventual death, and decreased cerebral blood flow and ischemia

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53
Q

what are the neurologic effects of increased ICP?

A

general–> diffusely increased ICP will cause headache (morning headache or headache that is worse in valsalva maneuvers), nausea, vomiting, papilledema, Cushing’s response (HTN, bradycardia)

focal–> paralysis, aphasia, cranial nerve palsy, drowsiness, apnea (dependent on area being compressed)

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54
Q

what happens in a case of acute, severe elevated ICP?

A

eventually the elevated pressure on focal areas of the brain will cause it to shift along the pathway of least resistance–> movement along pressure gradients so that parts of the brain HERNIATE into other compartments

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55
Q

list the 4 herniation syndromes we need to know

A
  1. subfalcine herniation
  2. midline shift
  3. tonsillar herniation
  4. uncal (transtentorial) herniation
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56
Q

what is a subfalcine brain herniation?

A

herniation of the FRONTAL lobe under the falx

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57
Q

what is a midline shift brain herniation?

A

movement of one hemisphere toward the other

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58
Q

what is a tonsillar brain herniation?

A

herniation of the cerebellar tonsils through the foramen magnum –> can compress the medulla and cause respiratory depression

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59
Q

what is an uncal brain herniation?

A

aka transtentorial brain herniation

herniation of the uncus (medial temporal lobe) through the tentorial hiatus and up against the brainstem

can compress CN III, the midbrain cerebral peduncle, and the PCA (leading to stroke)

MEDICAL EMERGENCY–> sign of imminent death

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60
Q

how do the presentations of increased ICP that occurs rapidly versus slowly differ?

A

increased ICP that occurs rapidly is generally an ACUTE emergency

increased ICP that occurs slowly will often have no neuro symptoms

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61
Q

what does the tentorium separate?

A

the cerebellum from the cerebrum

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62
Q

list the types of supretentorial herniation

A
  1. uncal
  2. central
  3. subfalcine
  4. transcalvarial
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63
Q

list the types of infratentorial herniation

A

upward (upward cerebellar or upward transtentorial

tonsillar (downward cerebellar)

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64
Q

there are 12 general steps to the examination of the unconscious patient… what are they?

A
  1. vitals (including HR, RR, BP, temp and O2 sat)
  2. glasgow coma scale
  3. general appearance
  4. pupils
  5. fundi
  6. spontaneous eye movement
  7. corneal “blink” reflex
  8. doll’s eye (oculocephalic) reflex
  9. oculovestibular (caloric) reflex
  10. gag reflex
  11. motor exam
  12. reflexes/plantar response
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65
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

their glasgow coma scale rating

A

less than 8 indicates severe head injury (chart is on another question)

decorticate–> arm flexion to stimulation, indicates lesion above red nucleus

decerebrate–> extension to stimulation. indicates midbrain or rostral pons lesion (this is a worse sign)

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66
Q

what is the red nucleus?

A

The red nucleus or nucleus ruber is a structure in the rostral midbrain involved in motor coordination. It is pale pink in color; the color is believed to be due to iron, which is present in the red nucleus in at least two different forms: hemoglobin and ferritin.[1] It comprises a caudal magnocellular and a rostral parvocellular part. It is located in the tegmentum of the midbrain next to the substantia nigra. The red nucleus and substantia nigra are subcortical centers of the extrapyramidal motor system.

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67
Q

in terms of the examination of the unconscious patient:

what are the 4 N’s to look at on general appearance? what are you looking for specifically for each one?

A

Noggin–> trauma is seen via raccoon eyes, battle’s sign, or hemotympany

Neck–> immobilize in trauma, otherwise check for meningitis

Nose–> smell for alcohol, acetone, toxins)

Needle–> look for track marks

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68
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

pupils

A
  1. size
    - remember: PSNS constricts pupils, SNS dilates them
    - pinpoint pupils–> SNS disruption below midbrain level
    - unilateral dilation–> uncal herniation pressing on CN III
    - bilateral dilation–> severe metabolic/toxic cause or bilateral CN III
  2. symmetry
    - asymmtery in coma indicates supratentorial tesion until ruled out
    - otherwise–> eye trauma, aneurysm, cycloplegic drugs etc
  3. reactivity
    - unilateral non-reactive indicates uncal herniation
    - bilateral non-reactive indicates the same things as bilateral dilation and some drugs
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69
Q

what do pinpoint pupils indicate on the exam of an unconscious patient?

A

SNS disruption below the midbrain level

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70
Q

what does unilateral pupil dilation indicate on the exam of an unconscious patient?

A

uncal herniation pressing on CN III

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71
Q

what does bilateral pupil dilation indicate on the exam of an unconscious patient?

A

severe metabolic/toxic cause or bilateral CN III

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72
Q

what does a unilaterally unresponsive pupil in an unconscious patient indicate?

A

uncal herniation

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73
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

fundi

A

look for papilledema and cessation of venous pulsations in ICP; hemorrhages

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74
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

spontaneous eye movements

A

look away from seizure focus, toward stroke

dysconjugate gaze indicates a brainstem problem

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75
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

corneal “blink” reflex

A

sensation via CN V1, motor via CN III

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76
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

dolls eye (oculocephalic) reflex

A

present if eyes move in orbit to remain fixed on ceiling, absent if eyes stay mid-gaze when turning the head to the side

indicates brainstem dysfunction/pseudocoma

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77
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

oculovestibular (caloric) reflex

A

put ice water in ear and look at the direction that eye go

  • nystagmus in both eyes with fast phase to side opposite water–> no coma, intact brainstem
  • slow deviation to the side of water–> brainstem and MLF are intact
  • ipsilateral eye only moves to cold water–> MLF lesion
  • no eye movement–> brainstem dysfunction (structural or toxic)
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78
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

gag reflex

A

sensation via CN IX, motor via CN X

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79
Q

in terms of the examination of the unconscious patient, what are you looking for/at when you examine:

motor exam

A

look at tone and symmetry

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80
Q

what are the 5 clinical levels of altered consciousness?

A
  1. lethargy
  2. stupor
  3. coma
  4. akinetic mutism
  5. locked-in syndrome
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81
Q

in the following level of altered consciousness, in what state are the

  1. eyes
  2. arousability of the patient
  3. content of consciousness of the patient?

lethargy

A
  1. eyes closed
  2. arousable
  3. mildly impaired content
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82
Q

in the following level of altered consciousness, in what state are the

  1. eyes
  2. arousability of the patient
  3. content of consciousness of the patient?

stupor

A
  1. eyes closed
  2. arousable with effort
  3. markedly impaired content
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83
Q

in the following level of altered consciousness, in what state are the

  1. eyes
  2. arousability of the patient
  3. content of consciousness of the patient?

coma

A
  1. eyes closed
  2. unarousable
  3. not applicable
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84
Q

in the following level of altered consciousness, in what state are the

  1. eyes
  2. arousability of the patient
  3. content of consciousness of the patient?

akinetic mutism

A

*presentation is secondary to frontal/basal forebrain dysfunction

  1. eyes open
  2. wakeful
  3. impaired
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85
Q

in the following level of altered consciousness, in what state are the

  1. eyes
  2. arousability of the patient
  3. content of consciousness of the patient?

locked-in syndrome

A

*presentation is secondary to basis pontis dysfunction

  1. eyes open
  2. wakeful
  3. normal
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86
Q

what is the glasgow coma scale? what are the 3 components and how are they ranked?

A
  1. eye opening
    - spontaneous 4
    - to speech 3
    - to pain 2
    - no response 1
  2. verbal response
    - alert and oriented 5
    - disoriented 4
    - speaking but nonsensical 3
    - moans 2
    - no response 1
  3. motor response
    - follows commands 6
    - localizes pain 5
    - withdraws to pain 4
    - decorticate flexion 3
    - decerebrate extension 2
    - no response 1

mild–13-15
moderate–9-12
severe–3-8

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87
Q

define seizure

A

abnormal neurologic functioning caused by abnormally excessive activation of neurons, either in the cerebral cortex or in the deep limbic system

slides: the clinical manifestation of an abnormal and excessive excitation and synchronization of a population of cortical neurons

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88
Q

define epilepsy

A

recurrent unprovoked seizures due to genetically determined or acquired brain disorder

it is not an appropriate term to use for seizures that occur intermittently and predictably after a known insult, such as EtOH intoxication and withdrawal

slides: a tendency towards recurrent seizures

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89
Q

What is the etiology of epilepsy in infancy and childhood

A

prenatal or birth injury

inborn error error of metabolism

congenital malformation

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90
Q

What is the etiology of epilepsy in childhood and adolescence?

A

idiopathic

genetic syndrome

CNS infection

trauma

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91
Q

What is the etiology of epilepsy in adolescence and young adulthood?

A

head trauma

drug intoxication or withdrawal**this one is a cause of acute seizures and not necessarily epilepsy

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92
Q

What is the etiology of epilepsy in older adult?

A

stroke

brain tumor

acute metabolic illness **cause of acute seizure not epilepsy

neurodegenerative

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93
Q

list seizure precipitants

A
  1. metabolic and electrolyte imbalance
  2. stimulantes (i.e cocaine)
  3. sedative or ethanol withdrawal
  4. sleep deprivations
  5. subtherapeutic or supratherapeutic AEDs
  6. hormonal variations
  7. fever or systemic infection
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94
Q

what is the pathophysiology of seizures?

A

seizures occur when the abnormal increased electrical activity of the initiating neurons activates adjacent neurons and propagates until the thalamus and other subcortical structures are similarly stimulated

when the ictal discharge extends below the cortex to deeper structures, the reticular activating system in the brainstem may be affected, altering consciousness

seizures are typically self limited–> at some point the hyperpolarization subsides and the burst of electrical discharge from the focus terminates

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95
Q

at the cellular level, why do seizures occur?

A

because of an imbalance between excitation and inhibition of neurons

excitations–> ionic: inwards Na+ and Ca2+ currents//neurotransmitters: glutamate and aspartate

inhibition–> ionic: inwards Cl- (GABAa), outwards K+ (GAGAb) currents//neurotransmitter: GABA

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96
Q

why do hyperexcitable networks occur?

A

as a result of:

  1. excitatory aconal sprouting
  2. loss of inhibitory neurons
  3. loss of excitatory neurons which would normally be driving inhibitory neurons (feed forward and feed back inhibition components)
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97
Q

how do you classify seizures?

A

they are either general or focal (partial)

generalizes seizures are abnormal neuronal activity in both cerebral hemispheres with loss of consciousness

focal/partial seizures are abnormal neuronal activity involving one cerebral hemisphere

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98
Q

list the types of generalized seizures

A
  1. absence (petit mal)
  2. tonic
  3. clonic
  4. tonic-clonic (grand mal)
  5. myoclonic
  6. atonic (drop attacks)
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99
Q

list the types of focal/partial seizures

A
  1. simple partial
  2. complex partial
  3. secondarily generalized
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100
Q

define absence/petit mal seizure

A

sudden onset and termination with impairment of consciousness only

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101
Q

define tonic seizures

A

tensing of skeletal muscles

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102
Q

define clonic seizures

A

cycles of muscle contraction and relaxation

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103
Q

define tonic-clonic/grand mal seizures

A

sequential occurrence of tonic and clonic phases, often preceded by an AURA

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104
Q

define myoclonic seizures

A

brief, involuntary twitching of a muscle or group of muscles

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105
Q

define simple partial seizure

A

consciousness is maintained

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106
Q

define complex partial seizure

A

impairment of consciousness

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107
Q

define secondarily generalized seizure

A

seizure that begins focally, and progressing to being generalized

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108
Q

what is status epilecticus?

A

defined as at least 30 minutes of persistent seizures or a series of recurrent seizures without intervening return to full consciousness

several authors have proposed shortening the time criterion from 30 min to 5 min

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109
Q

what are the two basic neural causes of seizures?

A

increased excitation, decreased inhibition or both

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110
Q

how does the body normally prevent hyperexcitable states?

A

normally there is feed back and feed forward inhibition to prevent these states

however, mechanisms that can generate abnormal hyperexcitable states are:

  1. excitatory aconal sprouting
  2. loss of inhibitory neurons
  3. loss of excitatory neurons which would normally be driving inhibitory neurons (feed forward and feed back inhibition components)
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111
Q

what is the foundation/idea behind anti-convulsant drugs (to treat seizures/epilepsy)?

A

decrease excitation or increase inhibition

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112
Q

list 3 anticonvulsant drugs whose MOA is to increase inhibition

A
  1. barbiturate
  2. benzodiazepines
  3. gabapentin
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113
Q

MOA of barbiturate?

A

increase inhibition

PROLONG GABA mediated Cl- channel openings

*some blockade of voltage gated Na+ channels

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114
Q

MOA of benzodiazepine?

A

increase inhibition

increase FREQUENCY of GABA mediated Cl- channel openings

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115
Q

MOA of gabapentin?

A

increase inhibition

increase neuronal GABA CONCENTRATION and enhance GABA mediated inhibition

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116
Q

list anticonvulsant drugs whose MOA is to decrease excitation

A
  1. phenytoin (dilentin)
  2. carbamazepine
  3. lamotrigine
  4. valproic acid
  5. ethosuximide
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117
Q

MOA of phenytoin (dilentin)?

A

decrease excitation

block voltage gated Na+ channels at high firing frequencies

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118
Q

what are some side effects of dilentin/phenytoin?

A

can cause hirsutism, gingival hypertrophy, facial coarseness, hair loss and weight gain

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119
Q

MOA of carbamazepine?

A

decrease excitation

Blocks voltage gated Na+ channels

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120
Q

MOA of lamotrigine?

A

decrease excitation

blocks voltage gated Na+ channels

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121
Q

MOA of valproic acid?

A

decrease excitation

blocks voltage gates Na+ channels

may enhance GABA transmission in specific circuits

good drug but TERATOGENIC so avoid use in women of child bearing age

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122
Q

what is a special consideration in the use of valproic acid?

A

good drug but TERATOGENIC so avoid use in women of child bearing age

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123
Q

MOA of ethosuximide?

A

decrease excitation

blocks low threshold, “transient” (T type) calcium channels in thalamic neurons

mainly used in CHILDREN

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124
Q

list 3 mixed action anticonvulsant drugs

A
  1. topiramate
  2. levetiracetam (keppra)
  3. oxcarbazepin (trileptal)
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125
Q

MOA of topiramate?

A

mixed action anticonvulsant

blocks voltage dependent Na+ channels at high firing frequencies

increases frequency at which GABA opens Cl- channels (at a different site than benzodiazepines)

antagonizes glutamate action at AMPA/kainite receptor subtype

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126
Q

MOA of levetiracetam?

A

aka keppra

mixed action anticonvulsant

reduces high voltage activated calcium currents

reverses inhibition of GABA and glycine gated currents

127
Q

MOA of oxcarbazepin?

A

aka trileptal

mixed action anticonvulsant

blocks voltage gated Na+ channels at high firing frequencies

exerts effects on K+ channels

128
Q

what is the main rehabilitation hospital for patients with brain injuries?

A

GF Strong

there are other smaller facilities with limited rehab, but GF Strong is the best facility for those with severe deficits whose prognosis is favorable

129
Q

what are the admission criteria for rehabilitation programs through GF Strong?

A

above 18 years old

resident of BC

medically stable

primary diagnosis of acquired head injury (trauma, CVA, hemorrhage)

requires the services of an interdisciplinary team

130
Q

what is the primary goal of head injury rehab?

A

to assist people to improve their independence and quality of life

treatment programs are designed to meet identified needs and functional goals of individual patients

131
Q

what common functional problems are treated by head injury rehab programs?

A
  1. mobility–> inability to walk, difficulty with coordination and balance, weakness or loss of joint movement, difficulty completing an independent transfer
  2. self-care–> inability to control bladder and bowel, inability to self medicate, difficulty bathing, dressing, grooming or eating
  3. IADLs–> inability to manage household, finances, unable to drive or access public transit
  4. neurological–> inability to swallow, problems with memory, though processes, decision making, or reasoning, difficulty communicating with others, emotional problems
  5. recreational/vocational–> inability to participate in sports, need for job modification or skill retraining
132
Q

what does the interdisciplinary team at GF strong consist of, for the rehab of head injured patients?

A

nurses

social worker

physio

OT

physician

speech and language pathologists

psychologist

recreation therapist

133
Q

define general anaesthesia

A

altered physiologic state characterized by loss of consciousness, analgesia, amnesia and inhibition of autonomic and sensory reflexes

134
Q

what are the pharmacokinetics of general anaesthesia?

A

anaesthesia is induced when critical concentration is reached int he brain (Pbr)

inhaled anaesthetic must travel down several concentration gradients:
delivered concentration–> inspired concentration–> alveolar concentration–> arterial concentration–> brain concentration

**the higher the blood/gas solubility, the higher the blood-gas partition coefficient, and the SLOWER the rate of induction

135
Q

how are blood/gas solubility, the blood gas/ partition coefficient and rate of induction of anaesthesia related?

A

the higher the blood/gas solubility, the higher the blood-gas partition coefficient, and the SLOWER the rate of induction

i.e high blood solubility of an anaesthetic is a “Waste” because it is wanted in the BRAIN not the blood

136
Q

what is the MOA of general anaesthetics?

A
  1. suppress excitable tissues by facilitating inhibition
    - increased GABAa receptor-mediated transmission
    - increased background “leak” K+ conductance
  2. inhibits excitation
    - decreased glutamate and ACh receptor mediated transmission
137
Q

what is the MAC for general anaesthetics?

A

MAC is the minimum alveolar concentration

1 MAC is the concentration of an inhaled anaesthetic in the alveoli at 1 atm that prevents movement in response to a painful stimulus in 50% of patients (essentially is EC50)

138
Q

how do inhaled anaesthetics affect the organs?

A

suppress all excitable tissues (CNS, PNS, cardiac, skeletal and smooth muscle)

139
Q

what % of brain tumours are benign?

A

50%

140
Q

can benign brain tumours be dangerous?

A

yes you can get recurrence and based on location they can cause death (ie “malignant by position”)–> this is different from benign tumours elsewhere in the body

141
Q

how does the cure rate for malignant brain tumours compare to tumours elsewhere in the body?

A

its lower

142
Q

what is the lifetime risk for a brain tumour?

A

1/200

143
Q

what types of brain tumours have the best prognosis? which ones have the worst?

A

well-circumscribed tumours often have a good prognosis, but it depends on location

diffuse tumours have no cure and a poor prognosis–> excision may somewhat prolong life but complete excision is impossible

144
Q

what is the etiology of brain tumours?

A

etiology of most is unknown

irradiation can cause meningiomas, gliomas and nerve sheath tumours

immunosuppression can cause primary CNS lymphoma

145
Q

list some risk factors for brain tumours

A
  1. sex
    - gliomas are 60% male, meningiomas are 70% female
  2. association between breast cancer and meningiomas (hormone receptors)
  3. genetic factors play a role
  4. occupation may be a risk factor
  • no convincing data for diet or trauma to be risk factors
  • cell phone use may be of concern
146
Q

list clinical features of brain tumours

A
  1. epilepsy
  2. headache
  3. raised ICP
  4. focal neurological deficit
  5. short history (CNS tumours are generally aggressive)
  6. primary tumours of the CNS rarely metastasize
  7. in adults, brain tumours are 70% supratentorial and 30% infratentorial; in kids its the opposite
147
Q

list prognostic features for brain cancer for both the patient and the tumour

A

patient: age, neurological impairment, Karnofsky score
tumour: type, grade, location

148
Q

list the 4 types of gliomas

A
  1. astrocytomas
  2. oligodendrogliomas
  3. ependymal cell tumours
  4. mixed gliomas
149
Q

how are gliomas classified by the WHO?

A

grade I–> circumscribed, localized

grade II, III and IV–> diffuse and infiltrative (based on presence of nuclear pleomorphisms, mitoses, capillary endothelial proliferation and necrosis)

150
Q

name a circumscribed, grade I astrocytoma

A

pilocytic astrocytoma

151
Q

name a grade II, grade III and grade IV astrocytoma

A

II: diffuse astrocytoma
III: anaplastic astrocytoma
IV: glioblastoma

152
Q

what is MGMT and how does it relate to gliomas?

A

MGMT is a DNA repair protein responsible for the major mechanism of chemo-resistance in gliomas

silencing this gene by alkylating agents has been associated with longer survival

153
Q

are oligodendrogliomas well circumscribed or diffuse?

A

diffuse tumours

154
Q

name two oligodendrogliomas

A
  1. oligodendroglioma (II)

2. anaplastic (malignant) oligodenroglioma (III)

155
Q

where would you find an ependymal cell tumour in an adult? in a kid?

A

adults–infratentorial

kids–supratentorial

156
Q

where do ependymal cell tumours often occur?

A

around the ventricles in the brain

157
Q

name two histological features associated with ependymal cell tumours

A

perivascular pseudorosettes

true ependymal rosettes

158
Q

name 4 ependymal cell tumours

A
  1. ependymoma (II)-> relatively well circumscribed but have small infiltrating projections that make them very difficult to excise
  2. anaplastic epenymoma (III)
  3. myxopapillary ependymoma
  4. subependymoma (I)
159
Q

are mixed gliomas diffuse or well circumscribed?

A

diffuse

160
Q

name two mixed gliomas

A

mixed oligoastrocytoma (II)

anaplastic oligoastrocytoma (III)

161
Q

what are PNETs?

A

Primitive Neuro-Ectodermal Tumours

162
Q

if there is a PNET in the cerebellum, what is it called?

A

medulloblastoma

  • most common posterior fossa tumour in kids (often in the vermis)
  • tendency to “seed” through the CSF
  • small blue cell tumour
  • 5 year survival 5–70%
  • amplification of MYCN gene indicated poor prognosis
163
Q

if there is a PNET in the cerebrum, what is it called?

A

neuroblastoma

164
Q

if there is a PNET in the retina, what is it called?

A

retinoblastoma

165
Q

if there is a PNET in the pineal gland, what is it called?

A

pineoblastoma

166
Q

name 3 tumours of cranial and spinal nerves

A
  1. schwannoma
  2. neurofibroma
  3. malignant peripheral nerve sheath tumour (MPNST)
167
Q

how many types of neurofibromatosis (causing neurofibromas) are there?

A

2–> neurofibromatosis types 1 and 2

168
Q

what is another name for neurofibromatosis type 1?

A

von Reckinghausen’s disease

169
Q

what is the mutation associated with neurofibromatosis type 1?

A

17q11

170
Q

how is neurofibromatosis type 1 inherited?

A

autosomal dominant

171
Q

what is the pathophysiology of neurofibromatosis type 1?

A

associated with defect in neurofibromimin (encoded by a tumour suppressor gene)

tumours in NF1: neurofibroma, optic gliomas, astrocytomas, meningioma and schwannoma (but not bilateral vestibular schwannoma)

172
Q

what is the mutation associated with neurofibromatosis type 2?

A

22q12

173
Q

what is the pathophysiology of neurofibromatosis type 2?

A

inactivation of schwannomin (merlin)

tumours in NF2: bilateral acoustic schwannoma, neurofibroma, astrocytoma, meningioma, ependymoma

174
Q

what % of cranial tumours are meningiomas?

A

15%

175
Q

are males or females more likely to get a meningioma?

A

females

176
Q

where are meningiomas usually located?

A

90% intracranial
9% spinal
1% other

177
Q

describe meningiomas

A

generally slow growing and well circumscribed

tend to spread into the skull not the brain

characteristic WHORLS and PSAMMOMA bodies

178
Q

what % of meningiomas are benign? atypical? malignant?

A

benign –85%

atypical –10%

malignant –5%

179
Q

what does recurrence of meningiomas depend on?

A

grade, completeness of surgical excision, presence or absence of brain invasion

180
Q

rank the pituitary adenomas from most common to least common

A
  1. prolactin
  2. GH
  3. ACTH
  4. null cell
  5. mixed
  6. FSH/LH
  7. TSH
181
Q

how common are primary CNS lymphomas?

A

rare

occur most often in the elderly or the immuno compromised

182
Q

describe primary CNS lymphomas

A

can be solitary or multifocal

differential diagnosis: toxoplasmosis vs. PML vs. lymphoma (treat for toxo first, if no response then biopsy)

183
Q

how do primary CNS lymphomas respond to steroids?

A

sensitive to steroids at first, but will always regress then recur

184
Q

what type of lymphoma do primary CNS lymphomas tend to be?

A

B cell

185
Q

what is the prognosis for primary CNS lymphomas?

A

very poor

186
Q

how common are metastatic tumours to the CNS? where do these mets usually spread to in the brain?

A

just as common as other types of brain tumours

usually spread to parts of the brain with the greatest blood flow–> superficial areas and cerebral hemispheres (supretentorial)

187
Q

what are the most common primary tumours that spread to brain?

A

lung

breast

skin (melanoma)

GI

188
Q

name CN IX

A

glossopharyngeal

189
Q

where does CN IX/glossopharyngeal nerve exit the brainstem?

A

posterolateral area of the medulla

190
Q

what modalities are included in CN IX/glossopharyngeal?

A 
GSA
GVA
SVA
SVE/BE
GVE
191
Q

what is the function of the GSA modality of CN IX/glossopharyngeal nerve?

A

general sensation from posterior 1/3 of tongue, tonsil, skin of external ear, internal surface of tympanic membrane, pharynx

192
Q

what is the function of the GVA modality of CN IX/glossopharyngeal nerve?

A

chemo/baroreceptors in the CAROTID BODY

visceral afferent info from the tongue and pharynx–> GAG reflex

193
Q

what is the function of the SVA modality of CN IX/glossopharyngeal nerve?

A

taste from posterior 1/3 of tongue

194
Q

what is the function of the SVE/BE modality of CN IX/glossopharyngeal nerve?

A

motor to stylopharyngeus muscle

195
Q

what is the function of the GVE modality of CN IX/glossopharyngeal nerve?

A

PNS to parotid gland

196
Q

name CN X

A

vagus

197
Q

where does CN X/vagus nerve exit the brainstem?

A

posterolateral area of the medulla

198
Q

what modalities does CN X/vagus nerve carry?

A

GSA

GVA

SVA

SVE

GVE

199
Q

what is the function of the GSA modality of CN X/vagus nerve?

A

sensory from posterior meninges, external acoustic meatus, skin posterior to ears

200
Q

what is the function of the GVA modality of CN X/vagus nerve?

A

sensory from larynx, trachea, esophagus, thoracic and abdominal viscera, stretch receptors in AORTIC ARCH, chemoreceptors in AORTIC BODIES

201
Q

what is the function of the SVA modality of CN X/vagus nerve?

A

special sensory from taste buds in epiglottis

202
Q

what is the function of the SVE modality of CN X/vagus nerve?

A

motor to pharyngeal muscles and intrinsic muscle of larynx

203
Q

what is the function of the GVE modality of CN X/vagus nerve?

A

PNS to smooth muscles and glands of pharynx, larynx and thoracic/abdominal viscera

cardiac muscle

204
Q

name CN XI

A

accessory

205
Q

where does CN XI/accessory nerve exit the brainstem?

A

posterolateral area of the medulla

206
Q

what modalities are carried by CN XI/accessory nerve and what do they do?

A

SVE–> sternocleidomastoid and trapezius

207
Q

what brain system is the neuroanatomical structure primarily responsible for arousal? where is it located? how does it manage arousal?

A

the ascending reticular activating system (ARAS)

located in the paramedian tegmental zone of the brainstem

input of somatic and sensory stimuli to the cerebral cortex is controlled by the ascending RAS and functions to initiate arousal from sleep

208
Q

can a coma result from only one affected cerebral hemisphere?

A

no usually both need to be affected

209
Q

what is necessary for arousal?

A

a completely intact brainstem–> if the ARAS is impaired, the cerebral cortex cannot be aroused and depressed consciousness or coma results

210
Q

what structures, essential to arousal/consciousness, are particularly vulnerable to toxins, metabolic derangements or mechanical injury?

A

insults to the cerebral cortex or brainstem can each independently cause depressed consciousness or coma

211
Q

list systemic/metabolic etiology of altered mental status/coma

A

see page 99 of the BB review notes!!!

  1. hypoxia
    - severe anemia or pulm disease
    - enviro/toxin like cyanide or near drowning
  2. disorders of glucose
    - hypoglycemia (i.e in chronic alcohol abuse, or excessive use of insulin)
    - hyperglycemia (i.e diabetic ketoacidosis, non-ketotic hyperosmolar coma)
  3. decreased cerebral blood flow
    - hypovolemic shock
    - cardiac problems (i.e arrhythmias, MI, congestive heart failure, pericaridal effusion)
    - infectious (septic shock, bacterial meningitis)
    - vascular/hematologic (i.e hypertensive encephalopathy, pseudotumour cerebri, hyperviscosity like in sickel cell, hyperventilation, DIC)
  4. metabolic cofactor deficiency
    - thiamine deficiency (wernicke-korsakoff)
    - folic acid (from chronic alcholol abuse)
    - niacin deficiency
  5. electrolyte/pH disturbance
    - acidosis, alkalosis
    - hyper or hyponatremia
    - hyper or hypocalcemia
    - hypophosphatemia
    - hyper or hypomagnesemia
  6. endocrine disorders
    -myxedema coma
    -hypopituitarism
    -addisons disease
    -cushings
    -pheochromocytoma
    hyper or hypoparathyroidism
  7. endogenous toxins
    - hyperammonemia (liver failure)
    - uremia (renal disease)
    - carbon dioxide narcosis
    - porphyria
  8. exogenous toxins
    - alcohols
    - acid poisons (salicylates, paraldehyde)
    - antidepressant meds (lithium, TCAs, SSRIs, MAOIs)
    - stimulants (meth/amphetamines, cocaine)
    - narcotics/opiates (morphine, heroin, codeine, oxycodone, meperidine, methadone, fentanyl etc)
    - barbituates, benzodiazepines, rohypnol, bromide
    - hallucinogens
    - herbs/plants (aconite, jimson weed, morning glory)
    - volatile substances (hydrocarbonds, nitrites, anaesthetic agents)
    - ketamine
    - penicillin
    - anticonvulsants
    - steroids
    - heavy metals
    - cimetidine
    - organophosphates
  9. disorders of temperature regulation/environmental temp
    - hypothermia
    - heat stroke
    - malignant hyperthermia
    - high altitude cerebral edema
    - dysbarism
  10. primary glial or neuronal disorders
    - adrenoleukodystrophy
    - creutzfeldt-jakob disease
    - progressive multifocal leukoencephalopathy
    - gliomatosis cerebri
    - central pontine myelinosis
  11. other disorders of unknown etiology
    - seizures
    - postictal states
212
Q

what are the dural reflections? what do they do?

A

the dural reflections are places where the inner dural layer is reflected as sheet-like protrusions into the cranial cavity.

these dural reflections compartmentalize the brain

the FALX CEREBRI separates the hemispheres

the TENTORIUM CEREBELLI separates the cerebrum from the cerebellum and brainstem

213
Q

why do herniations occur in the brain?

A

when intracranial volume and ICP increase beyond the compensatory capacities of the CNS (i.e shifting of CSF into spinal cord), cerebral herniations occur along the path of least resistance (i.e the U shaped free edge of the tentorium cerebelli)

214
Q

what is the pathyphysiology of an uncal herniation and how does this explain the symptoms associated with such a herniation?

A

occurs when the uncus of the ipsilateral temporal lobe hernaites and is compressed against the tentoruim

CN III is compressed leading to–> sluggish papillary reflex, impaired extraocular movements, pupillary dilation

ipsilateral peduncle compresses against the tentorium leading to–> contralateral hemiparesis and thus bilateral DECEREBRATE posturing (decorticate is not always present)

may also compress the PCA leading to PCA ischemic stroke

babinski’s sign is positive

if there is progressive herniation, you can proceed to brainstem compression and failure–> CV arrest–> death

215
Q

what is Kernohan’s phenomenon?

A

related to uncal herniations

usually, you get a situation where the ipsilateral peduncle compresses against the tentorium leading to–> CONTRALATERAL hemiparesis and thus bilateral DECEREBRATE posturing (decorticate is not always present)

however, in kernohan’s phenomenon, you can get CONTRALATERAL peduncle compression against the opposite edge of the tentorium, leading to IPSILATERAL hemiparesis

216
Q

what is cerebellotonsillar herniation?

A

cerebellar tonsils herniate through the foramen magnum

large central vertex mass (frontal or occipital pole) that forces brainstem displacement–> impingement of the MEDULLA–> SUDDEN respiratory and/or CV arrest

compression of the corticospinal tracts can cause FLACCID QUADRIPLEGIA

217
Q

in what situations would you order at CT for a patient after a witnessed traumatic loss of consciousness?

A

(canadian head CT rule)–>after a witness traumatic loss of consciousness, CT is only required for patients with any ONE of the following:

  1. glasgow coma scale score lower than 15 at two hours after injury
  2. suspected open or depressed skull fracture
  3. two or more episodes of vomiting
  4. 65 years or older
  5. amnesia before impact of more than 30 min
  6. dangerous mechanism

1-4 are “high risk for neurosurgical intervention”
5, 6 are “medium risk for brain injury detection by CT”

218
Q

name 4 specific types of closed head injury

A
  1. concussion
  2. brain contusion
  3. diffuse axonal injury
  4. intracranial hematoma
219
Q

what is a concussion?

A

any head injury that temporarily affects normal brain function

most concussions are mild and do not cause loss of consciousness but this is not always the case

220
Q

what are some immediate symptoms that might indicate concussion?

A

people suffering from a concussion can exhibit a number of immediate symptoms, including:

  1. headache
  2. dizziness
  3. nausea
  4. ringing in ears
  5. slurred speech
  6. vomiting

may also be confused, unable to concentrate, or have difficulty balancing

in some cases, sx do not surface until hours or days after the incident –> secondary sx include mood swings, sensitivity to light and noise, and changes in sleep patterns

221
Q

what is a brain contusion?

A

brain contusions are bruises of the brain tissue that occur as a result of brain trauma

in some cases, brain contusions lead to hemorrhages which are absorbed into brain tissue

if blood is absorbed into the CSF it can cause permanent neuro damage

are LOCALIZED–> distinguishes contusions from concussions which are more diffuse

222
Q

how do contusions and concussions differ?

A

contusions are localized whereas concussions are more diffuse

223
Q

in what % of brain injuries would you expect to find a brain contusion?

A

20-30%

224
Q

what are some symptoms of a brain contusion?

A

may feel weak and numb, lose coordination and struggle with memory or cognitive problems

225
Q

what is diffuse axonal injury?

A

one of the most debilitating traumatic brain injuries

frequently caused by high speed transportation accidents; sometimes associated with shaken baby syndrome

causes PERMANENT damage to nerves in the brain

may cause brain swelling and increased ICP

unlike more minor closed head injuries, severe diffuse axonal injuries lead to VEGETATIVE STATES or COMAS in 90% of patients

226
Q

what is an intracranial hematoma?

A

occurs when the brain is forced against the inside of the skull, resulting in a pool of blood outside the blood vessels of the brain or in between the skull and brain –> the brain is not designed to drain this much fluid!!

as a result, intracranial hematomas can compress brain tissue, requiring immediate medical attention

blood that collects in the brain, or in between the brain and skull, may lead to unconsciousness, seizures and/or lethargy

227
Q

what are the 3 types of intracranial hematoma?

A

intraparenchymal

subdural

epidural

228
Q

what is a subdural hematoma?

A

occurs when a vein ruptures between the brain and the dura matter

229
Q

what is an epidural hematoma?

A

caused by a rupture of a blood vessel between dura and skull

230
Q

what is an intraparenchymal hematoma?

A

occurs when blood collects within brain tissue

231
Q

list some potential complications that can arise from closed head injuries

A

a traumatic brain injury can put a patient at risk of developing a variety of complications, including increased ICP and swelling of brain

  • seizures
  • nerve damage
  • cognitive disabilities
  • communication difficulties
  • personality changes
  • changes in sensory perception
  • post concussion syndrome
  • coma

most patients suffering from mild closed head injuries report headaches, dizziness, and short term memory loss

a severe closed head injury can lead to death or cause a patient to remain in a permanent vegetative state

232
Q

what should be done immediately in the case of a head injured patient in order to give them the best chances for rehab?

A
  1. initially should receive a loading dose, then week long maintenance, of PHENYTOIN (dilantin) to decrease chance of seizures
  2. supportive tx of fever and hyperglycemia (which both increase neuronal death)
  3. head trauma patients who are asymptomatic/only have headache, dizziness, or scalp lacerations/who did not lose consciousness–> have a low risk for intracranial injury and may be discharged home without a CT
  4. patients with a hx of altered or lost consciousness, amnesia, progressive headache, skull or facial fracture, vomiting, or seizure have a moderate risk for intracranial injury and should undergo prompt head CT
  5. patients with depressed consciousness, focal neuro deficits, penetrating injury, depressed skull fracture or changing neurologic exam have high risk of intracranial injury and need immediate CT and observation
233
Q

what are the long term tools for rehabilitation of the head injured patient?

A
  1. physio
  2. OT–> improve ADLs and IADLs
  3. social work
  4. psychology
  5. vocational counselor
  6. chemical dependency team
  7. recreation therapist
234
Q

what neurotransmitter is associated with the Raphe nuclei in the brainstem?

A

serotonin (they are serotoninergic)

235
Q

what neurotransmitter is associated with the ventral tegmental area?

A

it is dopaminergic

236
Q

what neurotransmitter is associated with the locus ceruleus?

A

it is noradrenergic

237
Q

what is the locus ceruleus?

A

The locus coeruleus is a nucleus in the pons (part of the brainstem) involved with physiological responses to stress and panic

238
Q

what modalities does the reticular formation process?

A

the reticular formation in the brainstem receives and modifies afferent input from ALL sensory modalities

239
Q

in what part of the reticular formation would you find ARAS?

A

lateral zone

240
Q

what are the neuromodulators and what do they do?

A 
the neurotransmitter systems associated with ARAS, use neurotransmitters which are referred to/considered NEUROMODULATORS:
norepinephrine
dopamine
serotonin
histamine
ACh

each of these gives a QUALITY to the consciousness continuum and the conscious experience

**need to recognize these 5 neurotransmitters as being important for consciousness continuum (dont need to know detailed mechanisms)

241
Q

where does the lateral zone of the reticular formation receive input from?

A

sensory info from spinoreticular tract afferents from spinal cord

242
Q

where does the lateral zone of the reticular formation send information to? what is the information that goes to each?

A
  1. hypothalamus–> influences autonomic output
  2. thalamus–> influence cortical output
  3. aminergic and cholinergic nuclei–> to influence level of consciousness
  4. medial zone of reticular formation–> to influence output to spinal cord thru the medial zone
243
Q

what response/reaction is norepinephrine responsible for?

A

fight or flight

244
Q

where is norepinephrine manufactured?

A

locus ceruleus in the tegmentum of the pons projecting to thalamus and forebrain

245
Q

what does the locus ceruleus influence? (via norepinephrine)

A

arousal

attention

sleep/wake state

(also cognitive function, mood, pain)

norepinephrine allows a FOCUS on a specific task or sensory input–> helps suppress less salient inputs

246
Q

what happens if there is a lesion in the locus ceruleus?

A

low level of norepinephrine leading to low level of arousal

247
Q

which neuromodulator allows for focus on a specific task or sensory input, by suppressing less salient inputs?

A

norepinephrine produced in the locus ceruleus

248
Q

what would happen if you gave someone dopamine exogenously while they were asleep?

A

they would wake up and start looking around i.e “why am i awake, what do i NEED?” (because dopamine promotes exploratory behaviors towards positively rewarding stimuli)

249
Q

where are the dopaminergic neurons and where do they project to?

A

dopaminergic neuros in the ventral tegmental area (VTA) project to prefrontal cortex and limbic structures

250
Q

what are the dopaminergic neurons from the VTA responsible for?

A

BEHAVIOURAL arousal and waking

promote locomotor and exploratory behaviors toward positively rewarding stimuli (i.e food)

geared towards REWARD and MOTIVATION

251
Q

what happens when you get a lesion in the VTA?

A

dopaminergic neurons are affected

this affects ATTENTIVE AROUSAL–> one becomes less attentive and more indecisive

252
Q

where are the serotonin releasng neurons found? where do they project?

A

the RAPHE nuclei –> project to the thalamus, cortex, other NT systems in brainstem

253
Q

what does serotonin (from the raphe nuclei) do when you are conscious?

A

in consciousness, serotonin regulates a QUIET, WAKEFUL state–>
sense of wellbeing, anxiety and aggression is controlled while u are awake

allows you to be productive when you are in the wakeful state plus influences the SLEEP WAKE continuum

  • mood
  • aggression
  • sleep/wake
254
Q

what happens if you lack serotonin/lesion in raphe nuclei?

A

insomnia

255
Q

where would you find histamine releasing neurons and where fo they project?

A

histamine releasing neurons from the tegmentum of the MIDBRAIN project to the thalamus and cortex

256
Q

what does histamine do in the brain?

A

stimulates WAKEFULNESS

if you block histamine you lower your state of arousal–> thus with antihistamines you get drowsy

257
Q

where would you find ACh releasing neurons in the brainstem? where do they project to?

A

ACh is released from the tegmentum of the PONS–> fibres project to the thalamus and the cortex

258
Q

what does the ACh released from the tegmentum of the pons do?

A

increases THALAMOCORTICAL activation and arousal

turning on next target of consciousness info stream–> signals the thalamus which them signals the cortex

(thalamus acts as gatekeeper of into to cortex)

259
Q

what brain structure most correlates with STATE of consciousness?

A

thalamus –> determines how responsive you are to the environment

260
Q

what is the thalamic reticular nucleus? (TRN)

A

REMEMBER THE TRN!!

it is a grouping of neurons that covers the outside of the thalamus–> it is a reticular meshwork (like a fishnet stocking) –> an interconnected mesh of neurons

has dense reciprocal relationships with ARAS, other thalamic nuclei and cerebral cortical structures

it is one of the “other” nuclei associated with the thalamus (along with the intralaminar nuclei)… there are also relay nuclei and association nuclei in the thalamus

261
Q

what type of neurons are those found in the thalamic reticular nucleus? (TRN)

A

it is an interconnected network of GABAergic neurons–> thus it is an interconnected network of dense INHIBITION

262
Q

why is the thalamic reticular nucleus (TRN) important?

A

it is the GATEKEEPER OF CONSCIOUSNESS

it coordinates the synchronous firing (40 hz) between the cortex and the thalamus that is necessary for consciousness

263
Q

what is the “consciousness channel”?

A

the “consciousness channel” is a 40 hz channel between ARAS and the thalamus, and the thalamus and the cortex

neurons “speak” to each other on a 40 hz frequency, which is the channel encoding consciousness

other information (i.e how much skin is being touched) is processed simultaneously but on a different frequency–> the actual consciousness of the touch is processed on 40 hz

264
Q

why is the cortex important for consciousness?

A

required to establish SIGNIFICANCE and MEANING of conscious experience

synchronous and reciprocal communication with the thalamus and other cortical areas

265
Q

which parts of the cortex are most important for consciousness?

A

prefrontal and parietal cortical areas are important –> these areas decide what sensory information is important and they decide what to do about what you feel

both of these areas need to be fully functional and intact for the consciousness experience

266
Q

what does the parietal cortical area do relating to consciousness?

A

attention

awareness of self

awareness of extrapersonal space

267
Q

what does the prefrontal cortical area do in relation to consciousness?

A

directing and maintaining attention

morality

problem solving

adjusting behaviour to social norms

planning

working memory

deliberate decisions

**executive function over consciousness

**involved in our ability to associate self with society and societies expectations

268
Q

what are some important questions to ask in a patient presenting with seizures?

A
  1. are they seizures?
  2. if so, are they generalized or focal from onset?
  3. if focal, where do they originate from?
  4. what is the cause of the seizure?
  5. are antiseizure meds indicated?
  6. how is patient quality of life affected?
  7. can anything be offered beyond meds?
269
Q

what signs might indicate previous undiagnosed seizures in a patient on history?

A
  1. childhood staring spells, episodes of amnesia
  2. isolated aura
  3. bizarre nocturnal behavior
  4. myoclonic jerks
270
Q

what is the DDx for seizures?

A
  1. syncope–> neural or cardiogenic
  2. psychiatric–> panic attacks, fugue state, psychogenic non-epileptic events
  3. other neuro conditions–> migraine, paroxysmal movement disorder, sleep disorder, TIA, transient global amnesia (TGA), encephalopathy
271
Q

what is syncope?

A

loss of consciousness and postural tone caused by cerebral hypoperfusion with spontaneous recovery

can have:
1. neurally mediated–> vasovagal, reflex-mediated, autonomic, valsalva, carotid sinus syndrome, reflex anoxic)

  1. cardiogenic–> arrhythmias, cardiac structural anormalities
272
Q

what are some clues that a “seizure” is more likely psychogenic?

A
  1. precipitated by stress
  2. suggestible and distractible
  3. occur in wakefulness in the presence of a witness
  4. asynchronous asymmetrical movements–> pelvic thrusting, back arching, side to side head
  5. eyes closed with tightening upon attempted passive eye opening
  6. consciousness retained or fluctuating during “convulsion”
  7. crying
  8. intractable to anti-epileptic meds
  9. no post ictal confusion
  10. belle indifference (inappropriate lack of emotion usually regarding the event)
273
Q

what is the DDx for paroxysmal neurologic symptoms?

A

seizure

TIA

migraine

274
Q

what is the major test done for the investigation of seizures?

A

EEG

identify epileptiform activity (best sensitivity if done within 24 hours)

exclude non-convulsive seizures (in context of unexplained prolonged altered mental status)

275
Q

what is the status epilepticus treatment algorithm?

A
  1. lorazepam or midazolam
    - -after 0-30 min–
  2. phenytoin with cardiac and resp monitoring
    - -after 30-60 min–
  3. either valproic acid //or phenobarbitol //or ICU/intubate with bolus of midazolam or propofol, thiopental or pentobarbital infusions

(considered refractory status after step 2)

276
Q

which anti seizure med that we have to know is the only one that cant be used for both partial and generalized seizures?

A

lacosamide (vimpat)–only partial seizures

277
Q

what is the definition of drug resistant epilepsy?

A

failure of adequate trials of TWO tolerated appropriately chosen and used AED schedules (whether as monotherapy or in combo) to achieve sustained seizure freedom

278
Q

what are the indications for epilepsy surgery?

A
  1. drug resistant focal epilepsy–> goal is CURE with cessation of debilitating seizures
  2. drug resistant drop attacks and GTCs (i.e lennox gastaut syndrome)–> goal is PALLIATION with cessation of GTCs and drop attacks
279
Q

is “seizure” a diagnosis?

A

no its a symptom of underlying brain dysfunction –> epilepsy is a clinical diagnosis

280
Q

what are the three main determinants of cerebral blood flow? (CBF)

A

vessel radius (r)

pressure gradient (delta P)

blood viscosity (n)

281
Q

in what range of mean arterial pressures is a constant flow of blood to the brain maintained? how is this achieved?

A

between 50-160 mmHg mean arterial pressure–> via pressure autoregulation

pre-capillary arterioles dilate or constrict

this is myogenic–> via stretch sensitive Ca2+ channels

282
Q

how does Pco2 affect cerebral blood flow?

A

cerebral blood vessels are very sensitive to changes in Pco2

HYPERcarbia (hypoventilation) causes VASODILATION and INCREASED CBF

HYPOcarbia (hyperventilation) causes VASOCONSTRICTION and DECREASED CBF

these changes are mediated by extra-cellular H+ concentration

283
Q

how does Po2 affect cerebral blood flow?

A

CBF doesn’t vary much with changes in Po2 above 50mmHg

when Po2 falls below 50 mmHg, cerebral blood flow begins to rise exponentially

NO and adenosine (both vasodilators) are produced in response to cerebral hypoxia

284
Q

what cell type links cerebral blood flow and metabolism?

A

astrocytes

they send processes both to synapses and blood vessels, and communicate with other astrocytes through gap junctions

285
Q

in what type of seizures would you use phenytoin/dilantin?

A

partial seizures

secondarily generalized seizures

286
Q

side effects of valproic acid?

A

weight gain

menstrual irregularities

transient hair loss

tremor (rare)

287
Q

what anticonvulsant should be avoided in women of child bearing age? what is a good alternative?

A

valproid acid–>teratogen

alternative is lamotrigine

288
Q

what is a side effect of AED levetiracetim (keppra)?

A

potential behavior changes in some people who take this drug

i.e anxiety, agitation, mood swings, depression, suicidal ideation

289
Q

list AEDs that have shown efficacy for primary generalized epilepsy

A
  1. ethnosuximide
  2. valproic acid
  3. lamotrigine (keppra)
  4. levetiracetam
  5. dilantin (phenytoin)
290
Q

what is the meyer-overton rule of general anaesthetics?

A

an agent’s MAC inversely correlates with its lipid solubility–> the more lipid soluble an anaesthetic agent is, the more potent it is

291
Q

how do inhaled anaesthetics affect the CNS?

A

decrease in cerebral metabolic rate–> greatest with isoflurane

cerebral vasodilation–> increase in cerebral blood flow (N2O inly has a modest effect)

292
Q

how do inhaled anaesthetics affect the cardiovascular system?

A

decrease in arterial blood pressure as a result of reduction in cardiac output (i.e with halothane) and/or reduction in total peripheral vascular resistance (i.e isoflurane)

ventricular arrhythmias (halothane) –> “sensitization” of the myocardium to circulating catecholamines

N2O causes mild sympathetic stimulation

293
Q

how do inhaled anaesthetics affect the respiratory system?

A

respiratory depression–> increase in rate and decrease in depth of breathing (decreased tidal volume), net effect is a reduction in alveolar ventilation and elevation of Pco2, decrease in respiratory response to elevation in Pco2

decrease in airway resistance–> advantage for patients with asthma

294
Q

how do inhaled anaesthetics affect the kidneys?

A

reduction in renal blood flow leading to decreased in GFR and urinary output

295
Q

how do inhaled anaesthetics affect the skeletal muscle?

A

muscle relaxation

potentiation of the effects of nondepolarizing muscle relaxants (greatest with isoflurane)

296
Q

how do inhaled anaesthetics affect the uterus?

A

uterine relaxation (halothane and all other volatile agents)

may lead to prolonged uterine atony and severe blood loss in parturients

297
Q

list some characteristics about inhaled anaesthetics that make them so popular with anaesthesiologists

A
  1. ability to induce and maintain anaesthesia regardless of age or body habitus of the patient
  2. presence of clinical signs that give an indication of depth of anaesthesia
  3. ability to increase or decrease depth of anaesthesia at will
  4. a predictable pattern of recovery from anaesthesia
  5. provision of all of the components of the state of general anaesthesia in many patients without the use of adjuvants
  6. knowledge of the concentration of the drug at the site of action
  7. ability to deliver a broad range of oxygen concentrations
298
Q

what is an important difference between inhaled and IV anaesthetics?

A

the dose of an IV agent cannot be manipulated by the anaesthesiologist once injected

thus, their specific pharmanokinetic properties must be known

299
Q

name 4 IV general anaesthetics

A

thiopental

propofol

ketamine

etomidate

300
Q

what type of drug is thiopental?

A

IV general anaesthetic

barbituate (derivative of barbituric acid)

301
Q

what is the clinical use of thiopental?

A

rapid induction of hypnosis (NO ANALGESIA PROPERTIES)

302
Q

MOA of thiopental?

A

facilitation of inhibitory neurotransmission via GABAa receptors

303
Q

pharmacokinetics of thiopental?

A

rapid induction in one “arm-brain circulation time” (less than 20 sec

the brain concentration falls rapidly as a result of redistribution and thus the patient normally wakes up approx 5 min after a single bolus IV injection

when tissues are saturated, i.e as a result of continuous infusion or repeated doses, elimination and not redistribution determines the time of emergence

half life is 11 hours

304
Q

adverse effects of thiopental?

A

hypotension–> exaggerated in the presence of hypovolemia; dose reductions necessary in the elderly

respiratory depression

histamine release

arterial occlusion is possible

305
Q

clinical use of propofol?

A

the 1990s answer to thiopental

used for sedation, induction and maintenance of anaesthesia (TIVA–total intravenous anaesthesia)

smooth induction, “pleasant dreams”, rapid and clear headed awakening

antiemetic properties

306
Q

MOA of propofol?

A

facilitation of inhibitory neurotransmission via GABA a receptors

307
Q

pharmacokinetics of propofol?

A

rapid induction similar to thiopental, with even more rapid awakening (3 min after IV bolus)

rapid metabolism in the liver (half life of one hour)

no significant redistribution which is useful for infusion

308
Q

adverse effects of propofol?

A

pronounced hypotension (greater than thiopental, marked dose reductions necessary in the elderly)

respiratory depression and apnea

injection pain

potential for sepsis

309
Q

what is ketamine derived from?

A

its a PCP derivative

310
Q

what does ketamine do?

A

produces a state of “dissociative anaesthesia”–patient appears conscious, yet is unable to process or respond to sensory input (catatony, amnesia, analgesia)

produces little cardiorespiratory depression and maintains airway reflexes

has bronchodilator effect

unpleasant dreams are common

311
Q

clinical uses of ketamine?

A

induction of anesthesia in trauma or shock

battlefield surgery

analgesia in burn patients

i.m induction in kids

312
Q

MOA of ketamine?

A

antagonist at NMDA receptors (type of glutamate receptor)

313
Q

what type of receptor is the NMDA receptor?

A

glutamate

314
Q

pharmacokinetics of ketamine?

A

rapid induction after IV bolus (slower than propofol or thiopental)

hepatic metabolism with half life of 3 hours

B&B Part 1 (4 decks)

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