Week 29 head injury Flashcards
1
Q
Categories of neurotransmitters
A
Amino acids: glutamate, GABA, glycine
Peptides: Substance P, endorphins, enkephalins, ss, neuropeptide Y
Monoamines: serotonin, histamine, catecholamines
Other: Ach
2
Q
Discuss glutamate as a neurotransmitter
A
Excitatory
Memory & learning
3
Q
Discuss GABA and glycine as neurotransmitters
A
Inhibitory
GABA mainly in brain
4
Q
What do the peptide neurotransmitters bind to?
A
Opioid receptors in the brain.
Modulate pain, breathing.
5
Q
Discuss serotonin as a neurotransmitter
A
Inhibitory
Head: mood, impulsivity, sexual fntn.
Red: blood - platelet binding/adhesion
Fed: gut motility & nausea
MAO monoamine oxidase breaks down serotonin.
6
Q
Discuss histamine as a neurotransmitter
A
Excitatory in CNS
Wakefulness & alertness
7
Q
Discuss dopamine as a neurotransmitter
A
Excitatory
D - drive
O - psychosis
P - Parkinsonism
A - attention
M - motor
I - inhibition of prolactin
N - narcotics
8
Q
Discuss NE and Epi as neurotransmitters
A
Primary SNS excitatory
9
Q
Discuss Ach as a neurotransmitter
A
A - autonomic PNS, increases gut motility
C - contraction
H - hippocampus, memory
10
Q
Brain size vs energy needs
A
Brain is 2% of body but uses 20% of energy at rest
11
Q
What is the consequence of the high metabolic demand of the brain
A
Vulnerability to hypoxia.
Needs tight regulation.
12
Q
Neurovascular coupling
A
The spatial and temporal matching of changes in cerebral blood flow to changes in cerebral metabolism.
1. Match cerebral oxygen delivery to cerebral oxygen demain.
2. Remove metabolic byproducts such as CO2.
3. Regulated by neurons, astrocytes, and pericytes through multiple signaling pathways
Key driver seems to be NOS.
13
Q
Cerebral autoregulation
A
Regulation of cerebral blood flow by blood pressure.
Small range of pressure that maintains constant blood flow, but outside of that range, Blood flow : Blood pressure.
Brain in better able to respond to pressure increases than decreases.
14
Q
Cerebrovascular CO2 reactivity/Cerebral hypoxic vasodilation
A
Regulation of cerebral blood flow by blood gases.
Diameter of internal carotid changes by 20% in response to wide fluctuation of PaCO2. Doesnt happen in systemic circulation.
CO2 reactivity is greater with hypercapnia, then hypocapnia.
15
Q
Systemic vascular control vs Cerebral vascular control
A
Systemic: vascular resistance is regulated at the level of arterioles.
Cerebral: vascular resistance is regulated by every level of the circulation. 50% pressure lost before blood flow gets to pial arteries, d/t regulation from the internal carotid arteries.
16
Q
What structures regulate the remaining 50% of blood pressure?
A
Pial arteries, penetrating arteries, and capillaries. Capillaries also vasodilate in response to increased PaCO2.
17
Q
What is low CO2 reactivity in the brain associated with?
A
Increased risk of CV mortality and dementia.
18
Q
Where and how does CO2 act to effect blood flow?
A
Movement of CO2 through the blood vessel wall -> changes in CSF/perivascular pH -> changes in pial vessel diameter.
19
Q
What is the stimulus for changes in cerebral blood flow during hypoxemia?
A
O2 content (not PaO2).
Sufficient to maintain O2 delivery for hypoxemia, but not anemic hypoxia.La
20
Q
Lower limit of autoregulation in health individuals
A
appox. MAP >=70mmHg, but known to be variable.
21
Q
What happens to the curve of autoregulation in the setting of disease?
A
Shifts right.
LLA becomes greater than 70mmHg.
Greater risk for hypoperfusion in brain injury.
Current guidelines are to keep MAP >=65mmHg
22
Q
Classifications of TBI
A
Severity
Focal vs diffuse
Primary vs secondary
Blunt vs penetrating
23
Q
List the scoring components of the GCS
A
Eye opening:
4 Spontaneous
3 Verbal command
2 Pain
1 None
Verbal response:
5 Orientated
4 Confused
3 Inappropriate words
2 Incomprehensible sounds
1 None
Motor response:
6 Follows commands
5 Localizes to pain
4 Withdraws from pain
3 Flexes to pain
2 Extends to pain
1 None
24
Q
Discuss GCS scores
A
Must not have confounding conditions (hypothermia, drug tox/withdrawal)
Mild 12-15
Moderate 9-11
Severe <=8
Define each category with report: E4, V5, M6 = GCS of 15
If bilateral difference, use the higher score??
25
Discuss primary brain injuries
Hematomas
Contusions
Skull fracture
Diffuse axonal injury
26
Discuss how primary brain injuries can progress to secondary injury
Edema/blood from damaged tissues leads to increased ICP.
Increased ICP leads to ischemia.
Ischemia leads to:
Receptor mediated damage, Ca2+ mediated damage, Inflammation, Oxidative damage.
These lead back to further increased ICP and ischemia.
27
Focal vs diffuse injury
Diffuse: diffuse axonal injury
Focal: Subdural hematoma, Contusion, Epidural hematoma.
28
Monro-Kellie Doctrine
The cranial cavity is a closed rigid box and that therefore a change in the volume of one of the intracranial compartments can only occur as a result of a compensatory decrease in another compartment(s).
29
Volume with in the cranial cavity during normal ICP state
80% Brain
3-4% Arterial volume
6-7% Venous volume
10% CSF volume
30
Which components of cranial volume are first affected by increased ICP?
Veinous volume - gets pushed into thoracic compartment
CSF volume - gets pushed into spinal cord
Early injury leads to small pressure change, but once the veinous blood and CSF have been displaced, any small changes in volume lead to dramatic changes in pressure.
31
What is the outcome of late increased ICP from decompensation
Brain herniation
32
Cerebral blood flow equations
CBF = CPP/CVR [Cerebral perfusion pressure/Cerebral vascular resistance]
CBF = (MAP-ICP)/CVR [(Mean arterial pressure-Intracranial pressure)/Cerebral vascular resistance]
33
How does the cerebral blood flow equation help us?
Increases in ICP have inverse relationship to CBF. When ICP increases, CBF decreases. If we can keep ICP from increasing too much, we can maintain adequate CFB.
34
Cerebral O2 equation and the importance in managing brain injuries.
CDO2 = CBF x O2 content =(MAP-ICP)/CVR x O2 content
If we decrease CBF we decrease cerebral delivery of O2 which leads to secondary brain injury.
35
Where does the brain get its energy and why is this important?
Uses 25% of glucose in the body.
80-90% of ATP comes from oxidative metabolism.
So with decreased CD02, metabolism switches to anaerobic giving us only 2 ATP vs 36 from aerobic metabolism.
Without enough ATP, NA/K pumps no longer work. Na stays in the cells, H2O enters (following Na) and leads to edema. This further increases ICP and secondary brain injury.
36
What is the primary goal in management of primary brain injury and what is the overarching principle?
Prevent secondary brain injury.
Manage the balance of adequate CDO2 and having enough O2 for cerebral oxygen utilization without anaerobic metabolism.
37
Using the CDO2 equation list the ways we can manage adequate delivery of O2 to the brain.
CDO2 = (MAP-ICP)/CVR x O2 content
MAP: Maintain adequate perfusion pressure (systolic 90-100)
ICP:
Parenchyma = sedation (decreased metabolism), temperature control (decreased metabolism), Osmotherapy (Hypertonic Na/Mannitol; colloid pressure to pull fluid out)
CSF: ventricular drainage
Vascular: Arterial CO2 (manages vessel diameter, only used for active herniations.), venous drainage (cervical collars loose, bed elevation)
Mass Lesion: surgical resection, craniectomy
O2 content: Maintain hemoglobin (90 range), adequate O2 sat.
38
Which patients have ICP monitored?
Severe GCS >=8 (unconfounded)
Those with actionable pathophysiology
39
Normal and elevated ICP measurements
Normal: 7-15 mmHg
Elevated: >20-25 mmHg
40
Purpose of monitoring ICP
Detect catastrophic intracranial pathology
Monitor indicators of secondary injury
Target therapies
41
3 components of consciousness and the levels anatomical regions responsible for them
Level of consciousness: brainstem
State of consciousness: thalamus
Content of consciousness: cerebral cortex
All 3 components are required for normal consciousness
42
Which system within the brainstem determines the level of consciousness?
Recticular formation.
Made up of numerous nuclei within the brainstem.
Diffuse network of neurons with ascending and descending projections.
Receives and modifies afferent input form all sensory modalities.
43
Discuss the Ascending Reticular Activating System
Spinal cord brings all sensory info to reticular formation.
-> Hypothalamus for automonic output
->Medial zone of reticular formation for output to spinal cord
->Thalamus to influenc cortical output
-> Aminergic and cholinergic nuclei
44
List the 5 neurotransmitters involved in consciousness
NE
Dopamine
Serotonin
Ach
Histamine
45
Role of NE
From Locus Ceruleus in pons -> Thalamus and forebrain
Arousal
Attention and FOCUS
Sleep/wake
46
What happens if the Locus Ceruleus is damaged?
Low level of arousal
47
Role of Dopamine
From Ventral Tegmental Area ->Prefrontal cortex & limbic system
Motivation
Reward
Waking
*Behavioural arousal
D Drive
O PsychOsis
P Parkinonism
A Attention
M Motor
I Inhibition of Prolactin
N Narcotics (addiction)
48
What happens if the Ventral Tegmental Area is damaged?
Decreased attention and indecisiveness
49
Role of Serotonin
From Raphe Nucleus -> Thalamus, Cortex & Brainstem
Aggression
Mood
Sleep
Head : Mood
Red : Platelet binding
Fed : Gut motility/nausea
50
What happens if the Raphe Nucleus is damaged
Insomnia, aggression
51
Role of Histamine
Midbrain -> Thalamus & Cortes
Wakefulness
52
What happens if histamine release is impaired by damage to the midbrain?
Drowsiness
53
Role of Acetylcholine
Pons -> Thalamus & Cortex
Thalamocortical activation
Arousal
A Autonomic parasympathetic
C Contraction
H Hippocampus
54
What are the roles of the intralaminar nuclei and the thalamic reticular nucleus?
Critical for alertness and attention
TRN:
Gatekeeper of conciousness
Interconnected network of GABAnergic neurons
Coordinate synchronous firing between cortex and thalamus necessary for consciousness
55
Discuss how the thalamus is responsible for the state of consciousness
Thalamus receives input from sensory and determines responsiveness to the environment.
Utilizes association nuclei and relay nuclei (TRN)
TRN relays between thalamus, ARAS, and cerebral cortex.
56
Which part of the cortex is particularly important for the content of consciousness?
Frontal lobe.
Executive functioning/planning.
57
What will lesions in the frontal lobe result in?
Impulsiveness
Inattention
Decreased concentration
58
What type of content does the parietal lobe contribute to?
Self awareness.
59
Where do patients commonly develop contusions?
Frontal lobe.
60
What role does the cortex play in attention?
Allows us to have selective attention, selects a subset of information form the constant stream of information coming in.
61
What are the two broad forms of selective attention?
Top down:
Volitional control over the focus of attention.
Bottom up:
Rapid and automatic form of selective attention.
62
Role of prefrontal cortex as an association area
Executive function over consciousness.
More complex than other association areas.
Involved in out ability to associate self with society and societies expectations.
Disrupted in frontal lobe disease.
Plan future actions
Predict
Be attentive
Concentrate on a task
Discriminate between trivial and important
Behave appropriately
63
Autoreceptors
Sits on presynaptic neuron and is part of the negative feedback loop.
64
Heteroreceptors
Respond to neurotransmitters released by another cell.
65
Metabotropic receptors
2nd messenger systems.
Ex of 2nd messengers:
CGMP
cAMP
Inositol triphosphate
Ca2+
NO
66
Ionotropic receptors
Ion channels
67
What is required for NMDA channel opening
Activation by 2 ligands, glutamate & glycine and membrane depolarization to get rid of the Mg blocking the channel.
Non selective to + ions but preference for Ca2+
68
Which type of receptors dominate in the Raphae nucleus
HT-1a
69
Focusing apparatus of the eye
Main: Cornea
Less: Lens
70
Discuss the function of the lens when looking at something close up
Changes shape during accomodation to provide additional converging power.
71
Normal eye sight
Emmetropia
72
Nearsighted
Myopia
converging of light occurs before the retina
corrected by minus lens (concave)
73
Farsighted
Hyperopia
converging of light occurs behind the retina
corrected by plus lens (convex)
74
Different refractive powers in different axes
Astigmatism (football shape)
75
Loss of accommodative amplitude due to aging
Presbyopia
76
Additional questions for ocular history
VIPERPD
V vision
I irritation
P pain
E epiphora (tearing)
R redness
P past trauma
D diploplia
Plus past ocular hx, fam ocular hx, eyedrop use
77
Components of the eye exam
Visual acuity
Pupils
Eye movements
Confrontational visual field testing
External examination
Opthalmoscopy
Pressure (tonometry)
78
What does pinhole vision do?
Improves uncorrected refractive errors.
Can use it to narrow down lens/cornea vs neurological
79
Eye exam language
PERRL-APD
Pupils equal and round, reactive to light. Negative afferent defect.
80
Define seizure
The clinical manifestation of an abnormal and excessive excitation and synchronization of a population of cortical neurons.
81
Define epilepsy
A tendency toward recurrent seizures.
At least 2 unprovoked seizures occurring >24 hours apart.
One unprovoked seizure and a probability of further seizures similar to the recurrence risk after 2 unprovoked seizures (60% over the next 10 years).
82
Modes of seizure onset
Generalized
Focal
Unkown
83
Underlaying causes/etiologies of seizures
Genetic
Structural or metabolic
Unknown
84
Generalized seizures (types)
Most common:
Absence (blank out)
Tonic-clonic (grandmal)
Myoclonic (twitching of muscles)
Clonic (stiffening and contraction)
Tonic (rhythmic twitching)
Atonic (drop attacks)
85
Simple partial seizure
Focal/focal aware:
with motor signs
with somatosensory or special sensory symptoms (tingling)
with autonomic symptoms or signs (tachycardia)
with psychic symptoms (disturbance of higher cerebral function)
86
Complex partial seizure
Focal dyscongnitive/focal impaired awareness:
impaired consciousness
clinical manifestations vary with site of origin and degree of spreak (aura, automatisms, other motor activity)
duration of 1-2 mintues
87
Secondarily generalized siezures
Begins focally, with or without focal neuro symptoms.
Variable symmetry, intensity, and duration of tonic and clonic phases.
Duration 1-2 minutes.
Postictal confusion, somnolence, with or without transient focal deficits.
Warning before convulsion is sometimes a partial seizure.
88
Focal seizures
Origin in a specific area of the brain.
Can have awareness or impaired awareness.
Symptoms vary depending on the area of the brain involved.
Can stay localized or spread to other areas of the brain.
89
Generalized seizures
Origin is simultaneously both sides of the brain.
Typically involves a loss of consciousness.
Clonic, tonic, atonic, tonic-clonic, or absences seizures.
90
Etiology of seizures and epilepsy in infancy/childhood
Prenatal or birth injury
Inborn error of metabolism
Congenital malformation
91
Etiology of seizures and epilepsy in childhood/adolescence
Idiopathic/genetic syndrome
CNS infection
Trauma
92
Etiology of seizures and epilepsy in adolesence/young adult
Head trauma
Drug intoxication and withdrawal
93
Etiologo of seizures and epilepsy in older adult
Stroke
Brain tumor
Acute metabolic disturbances
Neurodegenerative
94
Precipitants of seizures
Metabolic and electrolyte imbalance
Stimulates
Sedative or EtOH withdrawal
Sleep deprivation
Antiepileptic medication reduction or inadequate treatment
Hormonal variations
Fever or systemic infection
95
Cellular mechanisms of seizure generation
Excitation:
Ionic - inward Na/Ca currents,
Neurotransmitter - glutamate, aspartate
Inhibition:
Ionic - inward Cl, outward K currents
Neurotransmitter - GABA
96
Glutamate role in epilepsy
Major excitatory neurotransmitter.
Ionotropic receptors (fast synaptic transmission) NDMA, AMPA, kainate receptors, gated Ca & Na channels.
Metabotropic receptors (slow synaptic transmission) modulation of synaptic activity.
97
What modulates glutamate receptors
Glycine, polyamine sites, zinc, redox sites.
98
GABA role in epilepsy
Major inhibitory neurotransmitter.
GABA a receptors: post-synaptic, linked to Cl channels
GABA b receptors: presynaptic autoreceptors, mediated by K channels.
99
Basic mechanisms underlaying seizures and epilepsy
Feedback and feed-forward inhibition to the granule cell in thalamus
100
Components of the GABA system
GABA receptor
Benzo receptor
Barbituate receptor
Cl channel
101
Syncope
Temporary loss of consciousness, caused by a fall in blood pressure.
Secondary to decrease in blood flow to the entire brain.
Fast onset
Short duration
Spontaneous recovery
No convulsion, not neurological (vs seizure)
102
Causes of syncope
Vasovagal syncope
Orthostatic hypotension (drugs/EtOh)
Cardiac causes (Dysrythmia, structural)
103
Acute management of seizure
Time with a watch
Don't hold them down
Cushion head, remove glasses
Loosen tight clothing
Turn on side
As seizure ends, offer help.
Observe, protect, prevent.
104
Meds for acute seizures
IV benzo
IV Dilantin (can be used 1/day)
105
Four common categories of sequalae from brain injury
Behavioural
Cognitive
Functional
Social
106
Penetrating injury
Brain is struck by a penetrating object (bullet)
107
Non penetrating injury
Acceleration/deceleration/rotational forces on the brain (MVI)
108
2 consequences (types of injury) from non penetrating injuries.
Diffuse axonal injury
Contusion
109
Most common tool for assessing brain injury
GCS
110
Post Traumatic Amnesia
Inability to lay down memories reliably from one day to the next.
Issues with orientation (time/place) and memory (three objects).
Abbreviated Westmead Post-traumatic Amnesia Scale
Orientation (name, place, reason, month, year) /5
GCS (eye/motor) /10
Memory (3 pictures) /3
111
Neuropsychiatric complications of TBI
Personality changes
Cognitive sequalae
Anxiety
Depression
Psychosis
PTSD
Substance use
Chronic traumatic encephalopathy
112
Personality changes d/t TBI
Impulsivity
Disinhibition
Aggression (unwarranted)
Lack of insight
113
Cognitive sequalae d/t TBI
Diffuse axonal injury -> generalized (attention/processing speed)
Focal injury -> Specific to area of brain affected.
114
Risk factors for psychosis post TBI
Male
Pre-injury mental condition
Family hx of schizophrenia
Injury severity
115
Chronic traumatic encephalopathy
Initially reported in boxers.
Cumulative repetitive TBIs over time.
Widespread tauopathy.
Frontotemporal volume loss, enlarged ventricles, substantia nigra degeneration, reduced brain mass.
Executive function and cognitive impairment (progressive).
Mood and behavioural disorders.
116
Progression of chronic traumatic encephalopathy
No symptoms (tau proteins form in frontal lobes and around blood vessels)
Anger, impulsivity, depression (tau protein spread across frontal lobe)
Confusion, memory loss (tau deposits extend to temporal lobes)
Severe cognitive deterioration (tau deposits spread all over the brain)
117
3 main components in management of neuropsych dt TBI
Neuro exam
Psych eval
Neuropsychological assessment.
Multidisciplinary management and rehabilitation, including family members.
118
What exacerbates neuropsych complications in TBI
lack of social support
119
Brain stem rule of 4
4 Midline structures that begin with M
4 Side structures that being with S
4 CN in medulla, 4 in Pons, 4 above Pons
4 motor nuclei in the midline divide equally into 12 (III, IV, VI, XII)
120
4 Midline brain stem structures that begin with M
Medial lemniscus (contralateral fine touch)
MLF (INO - midbrain)
Motor nuclei III, IV, VI, XII (tongue devation XII - medulla, eye deviation III, IV, VI - midbrain)
Motor corticopsinal tract (contralateral limb weakness)
121
4 Side brain stem structures that begin with S
Spinocerebellar tract (Iplilateral ataxia - pons/medulla)
Spinothalamic tract (contralateral pain/temp - entire brainstem)
Spinal nucleus of V ( loss of px/temp from face - entire brainstem)
Sympathetics (ipsilateral Horner syndrome - entire brainstem)
122
CNIX
Glossopharyngeal:
Taste (Post 1/3 of tongue - solitary nucleus and tract)
Visceral motor parasympathetic (parotid gland - inferior salivatory nucleus)
Somatic sensory (Pharynx, posterior oral cavity (trigeminal nucleus & tract)
Visceral sensory (Chemo/baro receptors in carotid body, gag reflex - solitary nucleus & tract)
Motor to pharyngeal arches (pharyngeal mm - nucleus ambiguous)
123
CN X
Vagus:
Motor to pharyngeal arches (pharyngeal mm - nucleus ambiguous)
Viceral motor parasympathetic (throracic/abdominal viscera - dorsal motor nucleus of vagus)
Visceral sensory (thoracic/abdominal viscera, aortic bodies/arch - solitary nucleus & tract)
Somatic sensory (meninges, pharynx, larynx - trigeminal nucleus & tract)
124
CN XI
Accessory nerve:
SCM/Trapezius
Corticobulbar tract for trapezius crosses over.
Corticobulbar tract for SCM stays ipsilateral
125
What exits through the jugular foramen?
CN IX, X, XI
126
CN XII
Hypoglossal
Intrinsic mm of the tongue, all bilateral UMN projections except for genioglossus (protrusion of the tongue)
UMN lesion - contralateral tongue deviation
LMN lesion - ipsilateral tongue deviation - lick the lesion
127
Brainstem reflexes on the unconscious patient
Pupillary light reflex (CN II, CN III - midbrain)
Corneal blink reflex (CN V, CN VII - pons)
Caloric testing (CN VIII - pons)
Pupillodilator reflex (sympathetics)
Gag reflex (CN IX, CN X - medulla)
Motor posturing: Flexor = above red nucleus -> lesion expands -> Extensor = involves/below red nucleus.
128
Significance of a blown pupil
Always a red flag that there is pressure on CN III - critical situation.
129
Pathway of corneal blink reflex
Trigeminal sensory nucleus -> Facial motor nucleus -> orbicularis occuli mm
130
Pathway of gag reflex
Sensory along CN IX -> Nucleus solitarius -> Nucleus ambiguous -> CN X -> closed glottis, elevated palate, contricted pharynx -> expelled irritant.
131
Where is the breathing centre located?
Medulla
132
Types of herniation in the brain
Subfalcine
Transtentorial (Uncal)
Foramen Magnum (tonsillar)
133
Subfalcine herniation
Raised intracranial pressure causes medial movement of cingulate gyrus.
Midline shift.
Most common type of herniation.
Leads to compression of ACA -> weakness of limb on contralateral side.
134
Transtentorial (Uncal) herniation
Increased intracranial pressure pushes brain tissue onto tentorium cerebelli.
Uncus of temporal lobe pushed onto CN III -> blown pupil, and cerebral peduncles -> contralateral weakness .
135
Tonsillar herniation
Increased intracranial pressure pushes cerebellar tonsils below foramen magnum, pushing on medulla.
136
Which type of herniation impacts the breathing centre?
Tonsillar.
Cerebellar tonsils push through foramen magnum and push on medulla.
137
Pathway of pupillary light reflex
Retina -> CN II -> Pretectal nucleus in midbrain -> bilateral Edinger-Westphail nuclei -> Parasympathetic fibers w/CN III -> ciliary ganglion -> short ciliary nerves -> contrictor pupillae
138
Pathway of dilator reflex
Emotion/sensory stimulus -> hypothalamus -> T1 sympathetics -> superior cervical ganglion -> postganglionic fibers w/carotid artery -> V1 -> orbit of eye -> Long ciliary nerves -> dilator pupillae
139
Convergence pathway
Vergence centre ->
Oculomotor nuclei ->
CN III ->
Medial rectus
140
Divergence pathway
Vergence centre ->
Abducens nuclei ->
CN VI ->
Lateral rectus
141
Accomodation reflex
Includes:
Convergence, thickening of the lens, pupil constriction.
Supraoculomotor area in midbrain controls this.
Supraoculomotor Area ->:
Bilateral Oculomotor nucleus -> convergence.
Bilateral Edinger-Westphal nucleus -> pupil constriction.
Parasympathetic -> ciliary muscles -> thickening of lens.
142
CN IX supplies:
Taste post 1/3 of tongue.
Sensation post 1/3 tongue, tympanic membrane, external ear, pharynx.
Motor to styopharyngeus.
Parasympathetic to parotid gland.
Visceral sensation from carotic body/gag reflex.
143
CN X supplies:
Motor to pharyngeal and intrinsic larynx mm.
Parasympathetic to viscera and larynx.
Somatic sensory from meninges, back of ear, larynx, pharynx.
Visceral sensory from larynx, pharynx, viscera, aortic bodies, carotid stretch receptors.
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