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The brainstem and cranial nerves

How the brainstem keeps us breathing and awake, what the twelve cranial nerves do, how they are tested, and what happens when they fail.

Intermediate · about 9 min · updated 2026-10-02 · awaiting clinical review

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Illustrative simulation excitatory inhibitory

The midbrain, pons and medulla and the tracts that pass through them; the twelve cranial nerves and the five shown as tracts in this atlas; arousal from the reticular formation and breathing from the pre-Bötzinger complex; the vestibulo-ocular reflex and head impulse test; brain death determination; Bell's palsy, trigeminal neuralgia, locked-in syndrome and covert consciousness; reflex gain, the apnoea–hypopnoea index and Kaplan–Meier survival; nerve stimulation and new tests.

Contents
  1. The stem of life
  2. What the brainstem and cranial nerves are
  3. Why the brainstem is vital
  4. How the brainstem is tested
  5. When things change
  6. When the brainstem and cranial nerves fail
  7. The mathematics of bedside measurement
  8. Technology: stimulators and new tests
  9. Milestones
  10. Frontiers
  11. Check yourself

The stem of life

The stalk at the base of the brain keeps you breathing and awake, and carries many of the pathways between brain and body. In 1991 a small region of the ventral medulla, the pre-Bötzinger complex, was found to contain neurons essential for generating the rhythm of breathing in newborn rats: remove it and the rhythm stops.[1]

Twelve pairs of cranial nerves leave the brain and brainstem to control movement and sensation in the head and neck. When the brainstem is damaged, people can lose movement and speech while remaining fully conscious; most of those surveyed after years in this locked-in state reported being happy.[2,3]

This reading covers the brainstem, the cranial nerves (five of them shown as tracts in this atlas), arousal and breathing, reflexes used at the bedside, what goes wrong, the mathematics of clinical measurement, and how stimulators and new tests are changing care.[2,4]

What the brainstem and cranial nerves are

Brainstem. The midbrain, pons and medulla contain the nuclei of most cranial nerves: for example, the oculomotor nuclei lie in the midbrain at the level of the superior colliculi; the abducens nucleus lies beneath the floor of the fourth ventricle in the dorsal pons; the facial motor nucleus is in the lower pons; and the vagus emerges from the lateral medulla.[2]

Long tracts pass through. Many of the atlas's tracts run through the brainstem, among them the corticospinal, corticobulbar and reticulospinal tracts, the medial lemniscus and the three cerebellar peduncles (inferior, middle and superior).[4,5]

Cranial nerves in the atlas. The tract atlas includes the optic, oculomotor, trigeminal, facial and vestibulocochlear nerves. The trigeminal is the largest cranial nerve; it leaves the lateral pons and splits into three divisions at the trigeminal ganglion.[2,4]

The twelve cranial nerves[2]
NerveMain rolesFibre types
I OlfactorySmell, from the nasal cavity to the olfactory bulbSpecial sensory
II OpticVision; nasal fibres cross at the optic chiasmSpecial sensory
III OculomotorFour eye muscles and the eyelid elevator; pupil and lens musclesMotor and parasympathetic
IV TrochlearSuperior oblique muscle onlyMotor
V TrigeminalSensation of the face (three divisions); muscles of masticationSensory and motor
VI AbducensLateral rectus muscleMotor
VII FacialMotor root; sensation from the front two-thirds of the tongue; lacrimal glandMixed
VIII VestibulocochlearHearing (cochlear nerve) and balance (vestibular nerve)Special sensory
IX GlossopharyngealPosterior third of the tongue (taste and sensation); oropharynx; stylopharyngeusSensory, motor and secretory
X VagusVocal cords via the recurrent laryngeal nerve; continues into the chest and abdomenMixed
XI AccessorySternocleidomastoid and trapezius musclesMotor
XII HypoglossalMuscles of the tongueMotor

Key numbers

Pairs of cranial nerves
12[2]
Approximate length of the optic nerve
about 50 mm[2]
Patients followed after microvascular decompression for trigeminal neuralgia
1,185[6]
Patients with covert consciousness among those with disorders of consciousness
up to 15–20%[7]

Why the brainstem is vital

Wakefulness. In 1949 Moruzzi and Magoun found that stimulating the reticular formation of the brainstem replaced the slow, synchronised electrical activity of the cortex with low-voltage fast activity, like an arousal reaction, through ascending impulses relayed to the forebrain.[8]

Breathing. Medullary slices containing the pre-Bötzinger complex generated respiratory-related oscillations like those of the whole brainstem, and contained neurons with pacemaker-like properties; the breathing rhythm may come from a population of such conditional bursting pacemakers.[1]

Gaze stability. The vestibulo-ocular reflex moves the eyes to compensate for head movements. When one horizontal semicircular canal is lost, a rapid head turn towards that side is followed by corrective saccades, a bedside sign described by Halmagyi and Curthoys.[9,10]

How the brainstem is tested

Brain death. Determining death by neurologic criteria follows a defined sequence: prerequisites must be met, a neurologic examination with defined components is performed, apnoea is tested, and ancillary tests have defined uses. A 2023 consensus guideline set out 85 recommendations covering adults and children.[11]

The head impulse test. A video system recording at 250 Hz measured the vestibulo-ocular reflex as accurately as the gold-standard search coils, detecting both overt and covert corrective saccades, and is easier to use in clinics, even in acute vestibular neuritis.[10]

Determining death by neurologic criteria (outline)Prerequisites metas set out in the guidelineNeurologic examinationits defined components,including brainstem functionApnoea testtests the drive to breatheAncillary test if neededused in the circumstances theguideline definesDeterminationby qualified clinicians,following the guideline
Determining death by neurologic criteria (outline). An outline of the components named in the 2023 consensus guideline; the full guideline defines each step and its exceptions. This is not a clinical protocol.[11]
Text version of the diagram
  1. Prerequisites met: as set out in the guideline. Leads to Neurologic examination.
  2. Neurologic examination: its defined components, including brainstem function. Leads to Apnoea test; Ancillary test if needed.
  3. Apnoea test: tests the drive to breathe. Leads to Determination.
  4. Ancillary test if needed: used in the circumstances the guideline defines. Leads to Determination.
  5. Determination: by qualified clinicians, following the guideline.

When things change

Within hours. In Bell's palsy, treatment with prednisolone started within 72 hours of onset improved the chance of complete recovery: at 3 months, 83.0% of patients given prednisolone had recovered facial function, against 63.6% of those who were not; acyclovir gave no benefit.[12]

Over years. After microvascular decompression for trigeminal neuralgia, most recurrences happened in the first two years; at ten years, 70% of patients were free of pain without medication, and the annual recurrence rate had fallen below 1%.[6]

Over a lifetime in locked-in syndrome. With appropriate care, people with locked-in syndrome can survive for decades, and a longer time in the condition was associated with happiness.[3]

When the brainstem and cranial nerves fail

Locked-in syndrome combines loss of speech and paralysis of all four limbs with preserved consciousness; vertical eye movements or blinking allow coded communication. Of 65 survey respondents with complete data, 47 reported happiness and 18 unhappiness, which was linked to anxiety and dissatisfaction with mobility, recreation and speech.[3]

Bell's palsy, an idiopathic facial palsy, is the most common cause of a unilateral peripheral facial neuropathy; reactivation of herpes simplex virus is the most probable cause, and the prognosis is often good.[2,12]

Trigeminal neuralgia (tic douloureux) is a facial pain syndrome. Microvascular decompression of the trigeminal nerve was safe and effective in a series of 1,185 patients, with two deaths (0.2%) and one brainstem infarction (0.1%) among the major complications.[6]

Covert consciousness. Some patients who appear unresponsive after brain injury are conscious: cognitive motor dissociation is found in up to 15–20% of patients with disorders of consciousness, and detecting it in intensive care predicts functional recovery at one year.[7]

The mathematics of bedside measurement

Three measurements from this reading show how numbers summarise brainstem function and treatment outcomes.[10,13,14]

Gain of the vestibulo-ocular reflex[9,10]
G=θ˙eye−θ˙headG = \frac{\dot{\theta}_{\text{eye}}}{-\dot{\theta}_{\text{head}}}

The ratio of eye velocity to head velocity, with the sign flipped because the eyes turn opposite to the head. A gain of 1 keeps the eyes perfectly steady on a target; a low gain, as after loss of a semicircular canal, leaves the eyes behind and must be corrected by saccades. Video and search-coil measurements of gain agreed closely.

Symbols in Gain of the vestibulo-ocular reflex
SymbolMeaningUnit
GGvestibulo-ocular reflex gain—
θ˙eye\dot{\theta}_{\text{eye}}eye velocitydeg/s
θ˙head\dot{\theta}_{\text{head}}head velocitydeg/s
Apnoea–hypopnoea index[13]
AHI=Napnoea+NhypopnoeaTsleep\mathrm{AHI} = \frac{N_{\text{apnoea}} + N_{\text{hypopnoea}}}{T_{\text{sleep}}}

The number of pauses and shallow breaths per hour of sleep; 15 or more indicates moderate-to-severe sleep apnoea. With upper-airway stimulation, the median AHI fell from 29.3 to 9.0 events per hour at 12 months.

Symbols in Apnoea–hypopnoea index
SymbolMeaningUnit
NNnumber of apnoeas or hypopnoeas—
TsleepT_{\text{sleep}}total sleep timeh
Kaplan–Meier survival estimate[6,14]
S^(t)=∏ti≤t(1−dini)\hat{S}(t) = \prod_{t_i \le t}\left(1 - \frac{d_i}{n_i}\right)

The probability of remaining free of an event (here, recurrence of pain) beyond time t, estimated from follow-up of different lengths. At each time t_i when events occur, it multiplies by the fraction of those still at risk who did not have the event. This is how the 70% ten-year pain-free figure after microvascular decompression was calculated.

Symbols in Kaplan–Meier survival estimate
SymbolMeaningUnit
S^(t)\hat{S}(t)estimated probability of being event-free beyond time t—
did_inumber of events at time t_i—
nin_inumber still at risk just before t_i—

Technology: stimulators and new tests

Stimulating a cranial nerve. In people with moderate-to-severe obstructive sleep apnoea who struggled with CPAP, an implanted upper-airway stimulation device, which stimulates the hypoglossal nerve to the tongue muscles, cut the median apnoea–hypopnoea index by 68% at 12 months in an uncontrolled cohort of 126 participants.[2,13]

Detecting hidden awareness. Advanced neuroimaging and electrophysiology can reveal preserved brain networks in patients who seem unresponsive, and new drug and electrical therapies are being tested to reactivate injured networks and promote the return of consciousness.[7]

EEG or fMRI signalsFeatures during commandsClassifierCommand-following?
Detecting covert consciousness (schematic). A schematic of how covert consciousness can be detected: brain responses recorded while a patient is given commands (for example, to imagine a movement) are compared with rest by a classifier; consistent differences suggest covert command-following.[7]

Imaging the nerves. Cranial nerves can be shown on MRI and computed tomography, and tractography can reconstruct several of them, as in the five cranial nerve tracts of this atlas.[2,4]

Milestones

From reticular formation to covert consciousness

  1. 1949Brainstem reticular stimulation is shown to activate the cortex.[8]
  2. 1958Kaplan and Meier publish their survival estimator.[14]
  3. 1988The head impulse sign of canal paresis is described.[9]
  4. 1991The pre-Bötzinger complex is identified as a likely generator of breathing rhythm.[1]
  5. 1996Long-term results of microvascular decompression for trigeminal neuralgia.[6]
  6. 2007Prednisolone shown to improve recovery in Bell's palsy.[12]
  7. 2009The video head impulse test is validated.[10]
  8. 2011Most people with chronic locked-in syndrome report being happy.[3]
  9. 2014Upper-airway stimulation for sleep apnoea.[13]
  10. 2021Covert consciousness in up to 15–20% of patients with disorders of consciousness.[7]
  11. 2023A unified adult and paediatric guideline for brain death determination.[11]

Frontiers

Finding the hidden patient. Detecting cognitive motor dissociation in intensive care predicts recovery at one year, raising hope for more accurate diagnosis and prognosis, although fundamental questions remain about which patients can recover.[7]

Clearer rules for brain death. The 2023 guideline integrated adult and paediatric guidance and added advice for extracorporeal membrane oxygenation, targeted temperature management and primary injury below the tentorium.[11]

Check yourself

Check yourself

  1. How many pairs of cranial nerves are there?
    Show answer

    Twelve pairs (24 nerves in all).

  2. Which region of the medulla is essential for generating the breathing rhythm in neonatal rats?
    Show answer

    The pre-Bötzinger complex.

  3. What did Moruzzi and Magoun find when they stimulated the reticular formation?
    Show answer

    The cortex switched from slow synchronised activity to low-voltage fast activity, like arousal.

  4. Which cranial nerve is the largest?
    Show answer

    The trigeminal nerve (V).

  5. What sign reveals loss of one horizontal semicircular canal?
    Show answer

    Corrective saccades after a rapid head turn towards the affected side.

  6. What fraction of patients recovered facial function at 3 months with prednisolone in the Bell's palsy trial?
    Show answer

    83.0%, against 63.6% without prednisolone.

  7. What is cognitive motor dissociation?
    Show answer

    Covert consciousness in a patient who appears unresponsive.

  8. What did most people with chronic locked-in syndrome report?
    Show answer

    That they were happy.

Glossary[1,2,3,6,7,8,9,11,13]

Brainstem
The midbrain, pons and medulla, connecting the brain with the spinal cord.
Cranial nerves
Twelve pairs of nerves that leave the brain and brainstem for the head and neck.
Reticular formation
A network in the brainstem whose stimulation activates the cortex.
Pre-Bötzinger complex
A region of the ventral medulla essential for breathing rhythm.
Vestibulo-ocular reflex
Eye movements that counter head movements to keep vision steady.
Locked-in syndrome
Loss of speech and limb movement with preserved consciousness.
Cognitive motor dissociation
Covert consciousness detected by brain measures in an apparently unresponsive patient.
Brain death
Death determined by neurologic criteria.
Microvascular decompression
Surgery that relieves pressure on a cranial nerve, used for trigeminal neuralgia.
Apnoea–hypopnoea index
Pauses and shallow breaths per hour of sleep.

References

  1. Smith JC, Ellenberger HH, Ballanyi K, Richter DW, Feldman JL. Pre-Bötzinger complex: a brainstem region that may generate respiratory rhythm in mammals. Science 1991;254(5032):726-729. doi:10.1126/science.1683005
  2. Romano N, Federici M, Castaldi A. Imaging of cranial nerves: a pictorial overview. Insights into Imaging 2019;10(1):33. doi:10.1186/s13244-019-0719-5
  3. Bruno MA, Bernheim JL, Ledoux D, Pellas F, Demertzi A, Laureys S. A survey on self-assessed well-being in a cohort of chronic locked-in syndrome patients: happy majority, miserable minority. BMJ Open 2011;1(1):e000039. doi:10.1136/bmjopen-2010-000039
  4. Yeh F-C. Population-Probability Atlas and Tract-to-Region Connectome (HCP-1065), data release. brain.labsolver.org 2022. https://brain.labsolver.org/hcp_trk_atlas.html
  5. Yeh FC. Population-based tract-to-region connectome of the human brain and its hierarchical topology. Nature Communications 2022;13(1):4933. doi:10.1038/s41467-022-32595-4
  6. Barker FG, Jannetta PJ, Bissonette DJ, Larkins MV, Jho HD. The long-term outcome of microvascular decompression for trigeminal neuralgia. New England Journal of Medicine 1996;334(17):1077-1084. doi:10.1056/NEJM199604253341701
  7. Edlow BL, Claassen J, Schiff ND, Greer DM. Recovery from disorders of consciousness: mechanisms, prognosis and emerging therapies. Nature Reviews Neurology 2021;17(3):135-156. doi:10.1038/s41582-020-00428-x
  8. Moruzzi G, Magoun HW. Brain stem reticular formation and activation of the EEG. Electroencephalography and Clinical Neurophysiology 1949;1(1-4):455-473. doi:10.1016/0013-4694(49)90219-9
  9. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Archives of Neurology 1988;45(7):737-739. doi:10.1001/archneur.1988.00520310043015
  10. MacDougall HG, Weber KP, McGarvie LA, Halmagyi GM, Curthoys IS. The video head impulse test. Neurology 2009;73(14):1134-1141. doi:10.1212/WNL.0b013e3181bacf85
  11. Greer DM, Kirschen MP, Lewis A, Gronseth GS, Rae-Grant A, Ashwal S, et al.. Pediatric and adult brain death/death by neurologic criteria consensus guideline. Neurology 2023;101(24):1112-1132. doi:10.1212/WNL.0000000000207740
  12. Sullivan FM, Swan IRC, Donnan PT, Morrison JM, Smith BH, McKinstry B, et al.. Early treatment with prednisolone or acyclovir in Bell's palsy. New England Journal of Medicine 2007;357(16):1598-1607. doi:10.1056/NEJMoa072006
  13. Strollo PJ, Soose RJ, Maurer JT, de Vries N, Cornelius J, Froymovich O, et al.. Upper-airway stimulation for obstructive sleep apnea. New England Journal of Medicine 2014;370(2):139-149. doi:10.1056/NEJMoa1308659
  14. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations. Journal of the American Statistical Association 1958;53(282):457-481. doi:10.1080/01621459.1958.10501452

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Template anatomy for education. Not patient-specific. Not for clinical decision-making.