CONTENTS
Neurological examination
- Global function & mental status
- Cranial nerves
- CN2,3 – Pupillary abnormalities
- CN3,4,6 – Extraocular movements
- CN5,7 – Corneal reflex
- CN9-Glossopharyngeal & CN10-Vagus
- CN11-Spinal Accessory nerve
- CN12-Hypoglossal nerve
- Motor exam & reflexes
- Sensory exam
- Miscellaneous
Neuroanatomy & Lesion Localization
- Cerebral hemispheres
- Brainstem anatomy
- Cerebellum
- Coma syndromes
- Questions & discussion
ability to follow commands?
- Ask to blink and to look up/look down (to evaluate for locked in state).
- Ask for unequivocal actions (thumbs up, show two fingers, close and open fist).
- 💡 Avoid asking to squeeze fingers, as this is potentially a grasp reflex. (Nelson, 2020)
ability to track or attend a stimulus?
- If eyes remain closed, gently open them (patients may have eyelid-opening apraxia).
- Apraxia of eyelid opening often occurs with non-dominant hemisphere lesions, but it can also occur with lesions in the medial frontal lobe, rostral brainstem, or basal ganglia (Parkinson's disease and Parkinson-plus syndromes).🌊
- Both eyes are affected.
- ? Ability to track a finger.
- The most potent visual stimulus is one's face. A smartphone may be used in selfie mode to determine if the patient will track to an image of their own face.
- ? Blink to threat (more on the blink reflex here: 📖).
how to examine
- For awake patients, ask them to move their extremities.
- For stuporous/comatose patients, apply painful stimuli to four extremities and bilateral face (e.g., supraorbital ridge, temporomandibular joints, or a Q-tip within the nose).
- Supraorbital pressure may be helpful, as this facilitates differentiation between localization versus withdrawal.
- A sternal rub may be less precise, but it provides very potent stimulation. This may be useful for patients who are unresponsive to less aversive stimuli.
- ⚠️ Sternal rub is contraindicated in patients status post recent surgical sternotomy.(Dunser 2019)
observe for
- Grimacing, for example:
- Grimacing without withdrawal may suggest an intact sensory response, with motor paralysis.
- Extremity flexion without grimacing in the lower extremity may be seen in the presence of brain death, due to a spinal reflex known as triple flexion. Triple flexion is also suggested if the patient responds exactly the same way, regardless of where their foot is stimulated (e.g., dorsum vs. sole).(24636925)
- Presence of any asymmetry (e.g., an asymmetric grimace or motor response implies the presence of a focal lesion).
- Motor responses to pain (listed below).
potential motor responses to pain
- Localizing to pain (GCS M5): Patient brings their hand towards the source of pain in a meaningful attempt to alleviate it. Examples of localization:
- (1) Stimulation of the supraorbital ridge or temporomandibular joint, causing the patient to bring their hand to their head.
- (2) Arm crosses midline, in efforts to alleviate a painful stimulus on the contralateral side.
- Withdraws to pain (GCS M4): The patient moves their arm in response to pain. This may include crude movements, or flexion of the arm towards the source of pain. The patient is able to move somewhat, but not in a meaningful way to evade the source of pain.
- Flexor posturing (decorticate; GCS M3) is loosely associated with damage at the level of the thalamus.
- Extensor posturing (decerebrate; GCS M2) is loosely associated with damage at the level of the midbrain. This may be associated with downward herniation, or compression of the brainstem by posterior fossa lesions. However, occasionally severe toxic/metabolic etiologies may also cause decerebrate posturing (e.g., hepatic encephalopathy); normal pupillary size and response may support a toxic/metabolic etiology.
- No motor response (GCS M1): Lesions below the pons may cause loss of all motor responsiveness (other than spinal reflexes such as triple flexion of the lower limbs).
how to observe breathing patterns
- Nonintubated patient: simple observation.
- Intubated patient: lift sedation (e.g., propofol) and place the patient on a pressure support mode (e.g., 10 cm pressure support with 5 cm PEEP). This allows patients to drive the rate and depth of respiration without interference, thus revealing their native breathing pattern.
- ⚠️ Localization is much less precise than has been suggested.(27907952)
Cheyne-Stokes respiratory pattern
- This is defined as a sinusoidal breathing pattern, reflective of a delayed feedback loop involved in regulating CO2 levels (e.g., commonly seen in severe heart failure with poor cardiac output). Generation of this pattern requires intact brainstem respiratory reflexes.
- Causes include:(Nelson, 2020)
- Heart failure with impaired cardiac output.
- Bilateral forebrain dysfunction (e.g., metabolic encephalopathies such as uremia, in which Cheyne-Stokes respiration is common).(Alpert 2019)
- Bilateral thalamic injury (e.g., downward transtentorial herniation).
- Acute stroke (especially extensive hemorrhagic stroke, but can occur with lacunar infarctions).(32924623)
central neurogenic hyperventilation
- Diagnosis requires an ABG/VBG that demonstrates a primary respiratory alkalosis.
- May be caused by various lesions:(27907952)
- (1) Midbrain or pontine lesions.
- (2) Bihemispheric lesions.
apneustic breathing
- This is a rare pattern that involves end-inspiratory pauses (figure above).
- Causes:
- Generally associated with bilateral pontine dysfunction (especially pontine infarction due to basilar artery occlusion).
- Rarely, may be seen in severe metabolic encephalopathies.(Alpert 2019)
cluster breathing
- Irregular clusters of breaths occur. This may mimic a Cheyne-Stokes pattern, but it lacks any smooth, sinusoidal transition between apnea and hyperventilation.
- Cluster breathing may reflect lower pontine or high medullary injury.
- Common causes include: stroke, cerebellar hemorrhage with brainstem compression, or anoxic encephalopathy.(32924623)
ataxic (Biot's) breathing
- Breaths have various amplitude and length, with interspersed periods of apnea.
- ⚠️ This suggests an unstable respiratory rate that may progress to apnea.(Louis 2021)
- Significance:
- May reflect damage to the dorsomedial medulla (e.g., as a component of Wallenberg syndrome 📖). This should always raise concern for a medullary infarct.
- Often occurs as a preterminal event due to medullary damage as a result of tonsillar herniation.(Alpert 2019)
hiccups
- May be associated with injury to the medulla (e.g., as a component of area postrema syndrome due to neuromyelitis optica spectrum disorders 📖 or in lateral medullary syndrome).
common signs of aphasia
- Paraphasias (substitution of one word for a similar word).
- Dysnomia (poor word retrieval).
- Abnormal speech fluency.
- Poor repetition (e.g., inability to repeat a sentence or phrase).
- Naming of objects is almost invariably impaired (regardless of the type of aphasia).(Albert 2019)
types of aphasia
- Broca's aphasia (nonfluent aphasia, with difficulty producing speech that frustrates the patient) – posterior inferior frontal lobe.
- Wernicke's aphasia (fluent, with poor comprehension) – superior temporal gyrus.
- Global aphasia – often due to a large lesion near the Sylvian fissure.
- Transcortical aphasias are marked by the ability to repeat normally, but deficiencies in either fluency or comprehension. These localize to areas outside of the perisylvian region.
- Alexia without agraphia (inability to read, yet able to write – aka “word blindness”).(27907952)
- Localizes to the dominant (usually left) medial occipital cortex involving the splenium of the corpus callosum. It is a disconnection syndrome that results from disruption of interhemispheric communication across the corpus callosum. Normally, visual information from the nondominant visual cortex must be transmitted across the corpus callosum in order to be decoded into language. Writing remains intact because the angular gyrus and associated expressive language centers (Broca area) are intact and connected.(18533088)
- Usually due to a PCA (posterior cerebral artery) stroke.
- If detected, this has strong localizing value.(18533088)
- Alexia with agraphia (inability to write or to read) – May associate with lesions in the angular gyrus, or with Wernicke's aphasia.(Albert 2019)
- ⚠️ It takes months for an aphasia syndrome to have reliable localizing value. In acute neurological disorders, precise subtyping of aphasia may not localize accurately.
(1) historical features to consider
- History of ocular trauma or surgery?
- Check old photographs (chronic anisocoria?, chronic ptosis?).
- Exposure to topical medications? (including nebulized ipratropium).
(2) determine if its a sympathetic lesion or a parasympathetic lesion
- Sympathetic lesion (e.g., Horner's syndrome):
- Anisocoria is greater in the dark (inability to dilate). This is especially noticeable within ~5-10 seconds of turning down the lights (dilation lag).
- Both eyes are briskly responsive to light (able to constrict).
- Small pupil is abnormal (unilateral miosis).
- This often implies the presence of Horner's syndrome (especially if there is also ptosis). More on the evaluation of possible Horner's syndrome below. 📖
- Parasympathetic lesion (e.g., CN3-oculomotor palsy):
- Anisocoria is greater in the light (inability to constrict).
- Larger pupil has a sluggish response to light (impaired constriction).
- Larger pupil is abnormal (unilateral mydriasis).
- This is discussed further immediately below 👇.
- (If anisocoria is similar in light or dark this suggests the possibility of physiological anisocoria).
(2b) unilateral parasympathetic lesion (mydriasis) – differential diagnosis
- (1) CN3-oculomotor dysfunction 📖. This is especially suggested if the involved eye is turned downwards and outwards (although external compression can affect pupil dilation before affecting eye movement). The dilated pupil may be sluggish, or entirely fixed/dilated. Causes include:
- (1) Herniation syndrome compressing the nerve sheath.
- (2) Midbrain lesion affecting the CN3-oculomotor nucleus.
- (2) Focal seizure.
- (3) Iatrogenic anticholinergic medication:
-
- Ipratropium got into the patient's eye (following nebulized administration).
- Patient touched their scopolamine patch and then rubbed their eyes.
- Dilated eye examination by an ophthalmologist.
-
- (4) Adie's tonic pupil:
- Isolated pupil dilation with light-near dissociation (reaction to accommodation is normal).
physiological anisocoria (benign variant) has the following features: 🌊
- (1) Degree of anisocoria is <1 mm.
- (2) Normal response to light and accommodation (this exonerates CN3).
- (3) Lack of ptosis.
- (4) Degree of anisocoria is similar in light and darkness (this exonerates the sympathetic system).
- (5) Chronic (may be seen on prior photographs, such as a driver's license).
oval pupil
- May indicate increased intracranial pressure (e.g., due to an acute hemispheric mass effect).(Wijdicks 2019) Ovoid pupils commonly precede anisocoria (unequal pupil size).(Dunser 2019)
- Oval or irregular pupils may be associated with midbrain pathology.(Alpert 2019)
RAPD (relative afferent pupillary defect, aka Marcus Gunn pupil)
- Usually caused by optic nerve pathology (or profound, extensive retinal disease).
- One pupil is less responsive to light, but does constrict when light is shone on the contralateral pupil (a consensual response).
- Swinging flashlight test: A flashlight is swung back and forth between the eyes, illuminating each eye for about two seconds. To avoid a near pupil response, the patient should fixate on a distant object and light should be shown on the eyes from below. The test is positive if the affected eye has reduced constriction and more rapid dilation (escape). In more severe cases, the affected eye may frankly dilate when light is shining on it.
- 🎥: Relative afferent pupillary defect
diagnosis of Horner's syndrome
- The classic features of Horner's syndrome are miosis, ptosis, and anhidrosis (small pupil, drooping eyelid, and lack of sweat). In critical care practice it's generally impossible to accurately determine the presence of anhidrosis, so this triad can be boiled down to the dyad of miosis and ptosis.
- Ptosis involves the upper and lower lids. Thus, the most accurate way to evaluate this is distance between the upper and lower eyelids (“palpebral length”).
- Examination in a darkened room may cause the normal pupil to dilate, thereby accentuating the difference between the pupils. The difference is greatest shortly after darkening the room (dilation lag; see the video below).
- Both pupils are briskly reactive to light (unlike anisocoria due to parasympathetic dysfunction).
- Examples:
differential diagnosis: other causes of unilateral ptosis
- Lesion of the CN3 (oculomotor nerve), which generally would be associated with a dilated pupil – more on this below.📖
- Weakness of the levator palpebrae superioris due to neuromuscular pathology (e.g., myasthenia gravis) or muscular pathology (e.g., ocular myopathy).
- Sagging eyelids in the elderly (blepharoptosis) or due to prior eye surgery.
causes of Horner's syndrome
- First-order nerves begin in the hypothalamus, travel through the lateral brainstem, and end in the intermediolateral column of the spinal cord (ciliospinal center of Budge).
- Second-order nerves travel from the spinal cord over the lung apex, to the superior cervical ganglion.
- Brachial plexus lesion.
- Cancer in the lung apex (Pancoast tumor).
- Thoracic surgery or chest tube placement.
- Third-order neurons travel from the superior cervical ganglion to the eye (running along the internal carotid artery and then through the cavernous sinus).
- Internal carotid artery dissection.📖
- Neck surgery.
- Cavernous sinus pathology.
bilateral dilated & fixed
- Bilateral midbrain damage causing loss of parasympathetic output from CN3-oculomotor (most often due to early transtentorial herniation).
- Extremely deep metabolic coma (e.g., hypothermia, barbiturates, bupropion, lidocaine, sympathomimetics).
- Anticholinergic drugs at high dose (especially atropine).
- Botulism. 📖
bilateral dilated & reactive
- Anticholinergic drugs.
- Withdrawal from alcohol or benzodiazepines.
- Sympathomimetics (e.g., amphetamine, cocaine, methamphetamines, MDMA).
- Serotonin syndrome.
- Generalized seizure, including the postictal period.
bilateral mid-position & fixed
- Bilateral midbrain damage with loss of sympathetic and parasympathetic output (most commonly seen after herniation, or in patients with brain death).
- Profound barbiturate coma (but not high doses of IV benzodiazepines or propofol).(27907952)
- Hypothermia.
bilateral mid-position & reactive (normal pupils)
- Normal pupils exclude a large lesion at the level of the midbrain. For a patient who is comatose, remaining possibilities include:
- (#1) Most likely, this may be toxic/metabolic coma, causing diffuse dysfunction of the cerebral cortex.
- (#2) Lesions in the dorsolateral, upper-mid pons.
- (#3) Bilateral thalamic dysfunction.
- Neuromuscular blocking medications (note that smooth muscles of the iris don't get paralyzed).
bilateral small pupils
- Medications (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors).
- Bilateral central Horner's syndrome:📖
- Usually due to extensive pontine hemorrhage (“pontine pupils”).
- May occur in the early phase of central herniation syndromes (either upwards or downwards herniation).
- Argyll Robertson pupils (bilateral small, irregular, and often asymmetric pupils that retain responsiveness to accommodation, but not to light; video example 🎥).
features of CN3 palsy
- (1) Pupil dilation – May be the first finding due to external compression of the nerve, since parasympathetic fibers run along the outside of the nerve.
- (2) Ptosis (CN3 supplies the levator palpebrae, which elevates the eyelid).
- (3) Eye position is down and out (due to unopposed actions of abducens and superior oblique muscles).
clues to further localization
- (1) Localization to the brainstem may be suggested by:
- Bilateral ptosis and bilateral superior rectus palsy (suggests lesion of the CN3 nucleus, given bilateral innervation of these muscles).
- Any sign of crossed long-tract findings, for example:
- (2) Pupil-sparing CN3-oculomotor palsy
- Intrinsic nerve micro-infarction due to diabetes/hypertension may cause abnormal eye position without affecting the pupils, because this affects the innermost fibers of the nerve. This clinical presentation is less worrisome for a mass lesion.
- However, another possibility that should be considered here is superior divisional CN3 palsy, which presents as ptosis and limited upward eye movement without pupillary involvement. This is most commonly associated with lesions in the anterior cavernous sinus or superior orbital fissure that compress the superior division of the nerve. However, other causes may include intrinsic brainstem disease, aneurysms, or leptomeningeal carcinomatosis.(32924623)
important causes of CN3-oculomotor dysfunction
- Brainstem lesions involving the CN3 nucleus.
- Damage to the nerve as it passes through the subarachnoid space:
- 🚨 Uncal herniation (usually ipsilateral). 📖
- Meningitis.
- Aneurysm of the posterior communicating artery, posterior cerebral artery, superior cerebellar artery, or internal carotid artery.(Alpert 2019, 32924623) Aneurysms of the anterior communicating artery or posterior cerebral artery may rarely cause contralateral CN3 dysfunction, possibly due to compression of the nerve against the tentorium.(32924623)
- Skull base tumors.
- Cavernous sinus disorder (additional nerves are usually involved including trochlear, abducens, and division V1 of the trigeminal).
- Other causes:
- Trauma
- Postoperative.
- Idiopathic intracranial hypertension.(32924623)
manifestation of CN6 palsy
- Inability to abduct the ipsilateral eye (i.e., temporal, or outward movement).
sub-localization of CN6 palsy
- Abducens nucleus lesion in the pons may be suggested by any of the following additional features:
- (1) Involvement of nearby CN7-facial, causing facial weakness.
- (2) Inability to adduct the contralateral eye (complete lateral gaze palsy 📖, due to damage to the pontine lateral gaze center).
- (3) Contralateral hemiparesis. If the pontine lesion also involves the corticospinal tract, eyes deviate away from the lesion (and toward the paretic limb). This is sometimes called “wrong way eyes,” since it is the opposite of the more commonly seen pattern which occurs with destructive lesions of the frontal lobe (wherein eyes look away from the paretic limb). Wrong way eyes usually indicate a contralateral pontine lesion involving the abducens nucleus, but this can also be caused by thalamic hemorrhage.(Berkowitz 2017)
- Abducens nucleus damage is a component of inferior medial pontine syndrome (Foville syndrome).📖
causes of CN6 palsy
- Increased intracranial pressure:
- Abducens nerve palsy is frequently a nonspecific sign of increased intracranial pressure. (This may result from any process that exerts downward pressure on the brainstem.)
- Elevated intracranial pressure may especially be suggested by bilateral CN6 palsies.
- (More on the diagnosis of elevated intracranial pressure here: 📖)
- Pontine pathology (additional abnormalities would usually be expected, as described above).
- Wernicke encephalopathy.
- Cavernous sinus lesion (should see other cranial nerves involved as well, especially CN3-oculomotor and/or CN4-trochlear).
- Meningitis, syphilis, or Lyme disease.
- Skull base neoplasm.
- Microvascular ischemia (e.g., diabetes, hypertension, smoking).
- Trauma.
- Multiple sclerosis.
neuroanatomy of horizontal gaze
- Gaze may be stimulated from the frontal eye fields, or as a reflex via the vestibular nerve (e.g., cold caloric reflexes).
- In both scenarios, gaze starts with CN 6 stimulating ipsilateral abduction. CN 6 communicates with the contralateral CN3 via the MLF (medial longitudinal fasciculus), to coordinate contralateral eye adduction.
how to test gaze abnormalities
- Awake & communicative patient: Ask the patient to follow your finger, or ask them to look to the right and the left. This stimulates a pathway involving the frontal eye fields and the PPRF (paramedian pontine reticular formation). It also requires the patient to have intact hearing and language comprehension.
- Comatose patients – oculocephalic reflex (doll's eyes):
- When the head is rotated, the eyes normally turn in the opposite direction (thereby staying fixated in roughly the same direction). This test shouldn't be performed in patients with C-spine injury (among whom cold caloric testing may be used instead).
- This is easily tested, as a front-line evaluation of eye movements in comatose patients. Intact oculocephalic reflexes argue strongly against a structural cause of coma. However, this reflex may be muted in deep metabolic coma, so symmetric absence of eye movements doesn't necessarily indicate a structural lesion.
- If the oculocephalic reflex is absent, cold caloric testing should be performed, since cold caloric testing provides a stronger stimulus to more rigorously evaluate eye movements.
- In awake patients, the oculocephalic reflex is overcome by voluntary gaze control.(24636925) If it's unclear whether an abnormal oculocephalic reflex is due to voluntary gaze control versus brainstem pathology, this may also be sorted out using cold caloric testing (discussed further below).
- Comatose patients – VOR (vestibulo-ocular reflex, aka cold calorics)
- This involves slowly flushing the ear with 50 ml of ice water, with the head of the bed inclined at a 30-degree angle (to properly align the semicircular canal). At least five minutes should be allowed to pass in between testing each ear.
- In a comatose patient with intact brainstem reflexes, this will cause the eyes to rotate towards the stimulated ear.
- ⚠️ Cold calorics may elicit nausea and vomiting in awake or mildly somnolent patients.
response to cold calorics often reveals an objective assessment of the patient's level of consciousness
- In patients without structural brainstem lesions, cold calorics will provide an objective determination of the patient's level of consciousness. This may be especially useful to expose states such as functional coma. Responses may be classified along a spectrum, as follows (Alpert 2019)
- #1) Completely normal response: Contralateral nystagmus occurs, without significant eye deviation. The cerebrum maintains complete control of eye position, albeit with some slow deviations (due to cold caloric stimulation) that are promptly corrected via nystagmus (fast-phase nystagmus occurs away from the cold ear). In a patient who appears to be clinically comatose, this unexpected finding would suggest functional coma (pseudocoma), malingering, or akinetic mutism.
- #2) Mildly abnormal response: Eyes deviate towards the cold ear, with contralateral nystagmus. The cerebrum loses control of eye position, but it is still attempting to drag the eye back to a normal position. This could be seen with bilateral hemispheric dysfunction causing lethargy or obtundation.
- #3) Ipsilateral eye deviation only: Eyes deviate towards the cold ear, without nystagmus. This reflects intact function of the brainstem, with no input from the cerebrum. Clinically this pattern may be seen in a patient with bilateral hemispheric dysfunction causing stupor/coma.
- #4) No response at all: Brainstem reflexes to caloric stimulation are mute. Absent vestibulo-ocular reflexes usually indicate brainstem pathology (e.g., this is seen in brain death). However, this may also be seen in very deep toxic/metabolic coma (e.g., phenytoin, tricyclic antidepressants, sedatives) or following administration of paralytics. Thus, the differential diagnosis here may include various brain-death mimics (more on these here 📖).
Below are some more common horizontal gaze abnormalities. These may be elicited when patients try to move their eyes, or by vestibulo-ocular reflexes.
frontal lobe damage causes a gaze preference
- Direction of the preference:
- Cortical damage (e.g., stroke) ➡️ Eyes deviate towards the lesion & away from the paretic limb.
- Focal seizure ➡️ Eyes deviate away from the lesion & towards the seizing limb. Active seizure can be associated with nystagmoid jerks. This may subsequently be followed by a Todd's paralysis, wherein the eyes deviate towards the paralyzed arm (mimicking a stroke).
- ⚠️ Postictal findings after a seizure will mimic those seen during a stroke.
- Eyes are able to cross the midline during cold calorics or doll's eyes maneuvers (thus, this is a gaze preference). In contrast, gaze paralysis is caused by brainstem lesions (more on these below).
peripheral lesion of CN6-abducens
- This causes an ipsilateral inability to abduct the eye (in response to any stimuli).
- More on abducens nerve (CN6) palsy: 📖.
lateral gaze palsy (damage to CN6-abducens nucleus or PPRF)
- Damage to the abducens nucleus in the pons causes an inability to gaze at all in the ipsilateral direction (i.e., both an inability to abduct the ipsilateral eye and an inability to adduct the contralateral eye).
- Unlike frontal lobe lesions, pontine lesions cause gaze paralysis, which cannot be overcome by the oculocephalic reflex or cold caloric stimulation.
- Further discussion of abducens nucleus damage: 📖.
- Damage to the PPRF (paramedian pontine reticular formation) would cause an identical pattern of abnormalities in response to volitional eye movements triggered via the frontal eye fields. However, PPRF damage wouldn't be expected to affect the oculocephalic or vestibulo-ocular reflexes.
INO (internuclear ophthalmoplegia, due to unilateral MLF damage)
- A lesion of the MLF impairs the ability of the ipsilateral eye to adduct.
- Convergence (bilateral adduction) is preserved, since this doesn't depend on the MLF pathway. Preservation of convergence demonstrates that the CN3 and medial rectus muscles are functional – they just aren't being triggered properly during horizontal gaze. (However, skew deviation can occur in patients with internuclear ophthalmoplegia, which may make it difficult to test convergence.)
- If the patient is awake, there may be nystagmus of the normal abducting eye (as if trying to tell the other eye to come along).(Berkowitz 2017)
- Causes of internuclear ophthalmoplegia include multiple sclerosis, pontine stroke, or tumor. Among patients <50 years old, multiple sclerosis is most likely.(Alpert 2019)
- 🎥: Internuclear ophthalmoplegia examples.
WEBINO (wall-eyed bilateral internuclear ophthalmoplegia, due to bilateral MLF damage)
- Clinical findings:
- Neither eye is able to adduct properly.
- Sometimes, the eyes may be abducted at baseline, creating a “wall-eyed” appearance.
- Differential diagnosis:
- Bilateral damage to the CN3 nuclei may cause a similar pattern, with inability of either eye to adduct. However, this would be expected to cause additional abnormalities (e.g., ptosis and pupil dilation – see the section on CN3 dysfunction: 📖).
- Progressive supranuclear palsy may present similarly, but vestibulo-ocular reflexes remain intact.(32924623)
- Causes: (32924623)
- Common causes: multiple sclerosis, brainstem tumor, or stroke.
- Less common causes: cryptococcus, neuromyelitis optica spectrum disorder.
- 🎥: WEBINO
one-and-a-half syndrome
- This results from a medial, dorsal (posterior), caudal pontine lesion that affects the CN6 nucleus and the ipsilateral MLF (e.g., Foville syndrome 📖).
- Clinical findings:
- (1) The only possible horizontal gaze is abduction of the contralateral eye towards the unaffected side. This often induces nystagmus in abduction.
- (2) Convergence is intact.
- (3) Patients often have ipsilateral facial weakness, due to involvement of the nearby facial nerve (CN7) nucleus. This may be termed an “eight-and-a-half” syndrome (i.e., 7+1.5 = 8.5).(Albin 2022)
- Causes: (32924623)
- More common: Ischemic stroke, demyelinating disease (e.g., multiple sclerosis), infection.
- Less common: Head trauma, mass lesions (e.g., brain tumors or arteriovenous malformations).
- 🎥: One-and-a-half syndrome
skew deviation (one eye looks up, other looks down)
- Skew deviation suggests a unilateral cerebellar lesion or a unilateral brainstem lesion (usually involving the CN8 nucleus). Asymmetric dysfunction of the vestibular system causes the brain to think the head is tilted when it is not.(Berkowitz 2017)
- In the context of a comatose patient, skew deviation may suggest a basilar artery occlusion.(Wijdicks 2021)
upward gaze may be caused by:
- Usually due to bihemispheric damage (e.g., following severe anoxic injury).
- Seizures.
- Brainstem injury. (Torbey, 2019)
- Oculogyric crisis.
downward gaze may be caused by:
- Bilateral hemispheric dysfunction (e.g., anoxic injury, metabolic coma).
- Thalamic injury (e.g., hemorrhage).
- Dorsal midbrain dysfunction (Parinaud syndrome – other findings & causes discussed below 📖).
- (Hydrocephalus is a common cause.)
horizontal conjugate roving eye movements
- General aspects:
- This refers to spontaneous, synchronized movements of the eyes back and forth. Some texts differentiate between “conjugate roving” versus “ping-pong” movements, but they seem to be fundamentally similar phenomena. Spontaneous roving eye movement is often seen in patients with a reduced level of consciousness.(Wijdicks 2019)
- These movements reveal normal function of midbrain and pons.
- Causes:
- (1) Bilateral cerebral hemispheric dysfunction. In the context of coma, horizontal conjugate eye movements exonerate the brainstem, thereby implying that the coma is due to bilateral cerebral hemispheric dysfunction (e.g., a toxic/metabolic coma). Severe bilateral hemispheric infarction can also cause this.(32924623)
- (2) Lesions in the cerebellar vermis may also cause horizontal conjugate roving eye movements (but such lesions in isolation wouldn't be expected to cause coma).(28187795)
- 🎥: Ping-pong gaze.
ocular bobbing or dipping
- Bobbing (rapid down, slow up) suggests a pontine lesion (video below).(28187795)
- Dipping (slow down, rapid up) might suggest bihemispheric dysfunction (e.g., anoxia or a metabolic disorder)(video below).(28187795) However, ocular dipping may be caused by a variety of lesions, so it lacks definitive localizing value.(Flemming 2022)
- 🎥: Ocular bobbing.
- 🎥: Ocular dipping.
nystagmus – see section below 📖
opsoclonus
- Opsoclonus is a dyskinesia marked by rapid, involuntary, chaotic, multidimensional conjugate eye movements without inter-saccadic intervals (“saccadomania” – example in the video below).(33232023)
- Differential diagnosis of opsoclonus:
- Ocular flutter is similar, but ocular flutter occurs only in the horizontal direction.
- Nystagmus may appear similar, but nystagmus involves both a fast (saccadic) phase and a slow phase.
- OMS (opsoclonus-myoclonus syndrome) is associated with paraneoplastic syndromes or viral infection (opsoclonus combined with myoclonus and/or ataxia, encephalopathy, generalized tremor).
- Causes of opsoclonus include the following (with the first three categories occurring most often):(Frucht 2022)
- Toxicologic: Amitriptyline, barbiturates, benzodiazepines, ketamine, lithium 📖, organophosphates, phencyclidine, phenytoin, salicylates, sympathomimetics (amphetamines, cocaine, serotonin syndrome), toluene, venlafaxine.
- Parainfectious: Often seen in younger patients, may associate with truncal myoclonus and ataxia. Causes include HIV, enterovirus, mumps, Zika virus, CMV, COVID-19.
- Paraneoplastic: Often seen in older patients; causes include small cell lung cancer, breast cancer, and ovarian cancer.
- Structural lesion:
- Stroke (may occur as a component of lateral medullary syndrome).
- Brain tumor.
- Brainstem encephalitis.
- Demyelinating disorders (including multiple sclerosis, neuromyelitis optica spectrum disorders, and MOG-IgG associated).
- Traumatic brain injury.
- Metabolic processes:
- Wernicke encephalopathy.
- Hyperosmolar hyperglycemic state.
Nystagmus is named after the fast phase. The differential diagnoses below focus on more acute and common forms relevant to critical care, without attempting to be comprehensive.(Frucht 2022)
central nystagmus (often due to brainstem pathology) 🌊
- Gaze-evoked, direction-changing nystagmus (e.g., right-beating when looking right; left-beating when looking left).
- Wernicke encephalopathy. 📖
- Antiepileptic agents.
- Alcohol, sedatives (intoxication is a common cause).
- Chiari I malformation.
- Downbeat nystagmus (usually accentuated by downward-lateral gaze).
- Cervicomedullary junction or cerebellar lesions; or less often pontine or medullary lesions (e.g., tumor, stroke, demyelination).
- Infection (e.g., West Nile encephalomyelitis).
- Wernicke encephalopathy. 📖
- Paraneoplastic.
- Medications (e.g., amiodarone, antiepileptic agents, lithium, opioids) or alcohol use.
- B12 or magnesium deficiency.📖
- Hydrocephalus.(32924623)
- Upbeat nystagmus (usually accentuated by upward gaze).
- Medullary lesions, or less commonly midbrain lesions (e.g., stroke, demyelination).
- Wernicke encephalopathy. 📖
- Paraneoplastic disorders.
- Convergence-retraction nystagmus – see Parinaud syndrome.📖
- Pure rotatory nystagmus (best noted by looking at the blood vessels in the sclera). This is most common with brainstem lesions involving the vestibular nuclei, especially medullary lesions as a component of Wallenberg syndrome 📖.(Alpert 2019)
- Pendular nystagmus (symmetrically oscillating eye movements with no dominant direction; usually congenital but can occur due to demyelination, following brainstem stroke, Whipple disease, or toluene abuse).
- 💡 Brainstem lesions are a more common cause of nystagmus than pure cerebellar pathology.(Alpert 2019)
seizure
- Seizures may cause horizontal nystagmus, with the fast phase directed contralateral to the epileptic focus.(Alpert 2019) This may be mediated by stimulation of frontal eye fields (discussed further above 📖).
- Nystagmus may last for the duration of the seizure. Most seizures are self-limiting within <5 minutes, so nystagmus would last for only a few minutes. However, patients with persistent NCSE (nonconvulsive status epilepticus) could experience ongoing nystagmus (more on nonconvulsive status epilepticus here: 📖).
- Other than during seizure, cortical lesions don't cause nystagmus.(Alpert 2019)
peripheral nystagmus
- Features:
- May be overcome by visual fixation.
- May be associated with ear pathology (e.g., hearing loss).
- Direction of the nystagmus is generally the same (with the fast phase towards the normally functional side). However, vestibular disease may cause direction-changing positional nystagmus in supine patients, wherein the direction of the nystagmus varies depending on which ear is facing downward.
- Nystagmus may be either horizontal or a combination of horizontal and rotatory (clockwise when the fast phase is to the left or counterclockwise when the fast phase is to the right).(Alpert 2019)
- Nystagmus is most marked when looking away from the lesion (looking in the direction of the fast phase).
- No features of additional brainstem pathology.
- Peripheral nystagmus is caused by lesions of the semicircular canals within the ear or CN8-vestibulocochlear (e.g., Meniere's disease, vestibular neuronitis, benign paroxysmal positional vertigo).
functions of CN5-trigeminal
- Facial sensation.
- Numb chin syndrome is often a manifestation of multiple sclerosis or systemic malignancy.(32924623)
- Muscles of mastication (each trigeminal nucleus is innervated bilaterally by the motor cortex, so unilateral lesions in the motor cortex usually cause no deficit in jaw movement).(Blumenfeld 2022)
involvement in reflexes
- The V1 division of the trigeminal nerve is involved in the corneal reflex: 📖.
- The jaw jerk reflex involves purely CN5-trigeminal (which mediates both afferent and efferent limbs). The jaw jerk is normally absent or minimal. A brisk jaw jerk reflex suggests bilateral upper motor neuron pathology, above the level of the trigeminal motor nuclei (as may be seen in amyotrophic lateral sclerosis or diffuse white matter disease).(Alpert 2019; Blumenfeld 2022)
- 🎥: Jaw jerk reflex.
The primary function of the facial nerve is to innervate the facial musculature. The facial nerve is involved in the efferent limb of the corneal reflex (discussed further below 📖).
upper motor neuron lesion (e.g., motor cortex)
- Clinical effects:
- Weakness predominantly involves the lower face. (The forehead receives bilateral innervation from both cortical hemispheres, so it is spared.)
- Emotional expression (e.g., spontaneous smiling) may be preserved, because the frontal lobe and extrapyramidal systems also provide stimulation to the facial nucleus. However, patients may be unable to smile upon command!
- Caused by any lesion within the corticobulbar tract that lies above the facial nucleus (e.g., the motor cortex).
lower motor neuron lesion (facial nerve or facial nucleus in brainstem)
- Clinical effects:
- Weakness of the entire ipsilateral face.
- Hyperacusis.
- Causes:
- A lower motor neuron lesion usually indicates a lesion within the facial nerve (e.g., Bell's palsy).
- However, a lower motor neuron lesion can involve the cranial nerve nucleus, or the nerve fascicle as it exits the brainstem – so this can occur in the context of brainstem pathology. Lesions of the facial nucleus usually localize to the posterior, inferior pons (e.g., Foville syndrome 📖 or Marie-Foix syndrome 📖).
neuroanatomy
- The afferent limb involves the ophthalmic division of the trigeminal nerve (V1). The efferent limb of the reflex occurs via CN7-facial.
- Stimulating one eye should elicit blinking bilaterally.
eliciting the corneal reflexes
- Dropping saline from a sterile saline flush is the kindest and gentlest approach to eliciting corneal reflexes. If this succeeds in eliciting corneal reflexes, then it may be concluded that the patient has intact corneal reflexes.
- Gently touching the edge of the cornea with gauze provides a stronger stimulus to elicit corneal reflexes, so this may be used if there is doubt about the reflex. Ensure that you are truly touching the cornea (rather than the sclera of the eye).
interpretation
- ⚠️ The corneal reflex may be sensitive to sedation.
- Unilateral pontine injuries may cause an ipsilateral loss of the corneal reflex. (Nelson, 2020)
- If the contralateral eye blinks but the ipsilateral eye does not, this indicates an ipsilateral facial nerve (CN7) paralysis.
- Bell's phenomenon: Conjugate upward deviation of the eyes without eyelid closure. Normally the eyes often elevate when they close, but we are unable to observe this. Seeing the eyes elevate indicates intact sensation (CN5) and intact pathways to CN3 (to elevate the eye), with dysfunction of the eyelid (CN7) – essentially revealing a CN7 palsy.(Torbey, 2019)
- Corneomandibular reflex (aka corneal pterygoid reflex or Wartenberg reflex):
- Jaw deviates away from the side of corneal stimulation, along with bilateral eye blinking.
- Implies a structural lesion injuring the trigeminal nucleus above the mid-pons level.(Torbey, 2019) Potential causes include herniation, intrinsic upper brainstem lesions, amyotrophic lateral sclerosis, or multiple sclerosis.
- 🎥: Corneomandibular reflex
blink to visual threat
- Involves: Optic nerve, a functioning visual cortex, and the facial nerve (CN7).
- (Shown in a video here.)
blink to auditory stimulus (aka, acoustic reflex)
- Tested by applying a loud auditory stimulus near the patient (e.g., clap).
- Unlike a visual threat, this does not require signal processing in the cortex. The acoustic loop runs through the brainstem. Thus, patients in persistent vegetative state may blink after a sound – without awareness of the sound.(Wijdicks 2019)
CN9 and CN10 generally function as a single entity
- CN9 and CN10 lie in very close proximity, with disease processes often involving both nerves. For example, motor fibers of both nerves originate from the nucleus ambiguus in the medulla.
- It's difficult to separately examine CN9 vs. CN10 during a basic neurologic examination, since their functions overlap.
- For general clinical purposes, it's reasonable to consider CN9/10 as a single functional entity.
functions of CN9/10
- Pharyngeal sensation and musculature (swallowing).
- Laryngeal muscles (speaking, mostly via the recurrent laryngeal nerve which is a branch of CNX-vagus).
- Aortic arch and carotid artery baroreceptors.
- CN10-vagus provides parasympathetic innervation to the heart, lung, and upper gastrointestinal tract.
clinical examination of CN9/10:
- Soft palate movement with phonation (saying “ahh”).
- Symmetric upward movement of the uvula suggests intact function of CN9/10.
- Unilateral damage to CN9/10 causes the uvula to be pulled towards the normal side.
- Bilateral damage to CN9/10 causes the uvula to remain immobile; this may correlate with dysphagia (especially with liquids).(Alpert 2019)
- Voice:
- CN10-vagus innervates the vocal cords.
- Lesions to CN10 may be suggested by a breathy, nasal, or hoarse voice. (However, dysarthria may result from abnormalities in CN 5, 7, 9, 10, or 12 – so this isn't necessarily specific to a lesion of CN10).
- Cough reflex (among intubated patients):
- CN10-vagus is required for the afferent pathway of the cough reflex (section below).
basics of the cough reflex
- The cough reflex involves the vagus nerve (CN10, near the medulla). This reflex will be preserved in most coma states (which usually involve higher brain centers).
- Reliably eliciting the cough reflex requires an intubated patient, in whom endobronchial stimulation can be applied by suctioning the endotracheal tube.
- The cough reflex is one of the most durable reflexes, which is generally preserved even in severe brain injury. For example, following anoxic brain injury, lack of a cough reflex after 24 hours carries a likelihood ratio of 85 for poor neurologic outcome.(14970067)
causes of an absent cough reflex include
- Damage to the medulla (e.g., tonsillar herniation, brain death).
- Extremely profound toxic/metabolic coma (e.g., barbiturate or baclofen overdose).
- Neuromuscular paralysis (e.g., lingering effects of rocuronium used for intubation).
💡 When encountering a patient who lacks a cough reflex without any obvious cause, always consider the possibility of a lingering neuromuscular paralytic agent. If the patient otherwise appears paralyzed (e.g., absent deep tendon reflexes), this should be immediately evaluated at the bedside using a peripheral nerve stimulator.
⚠️ please stop gagging patients
- The gag reflex will almost never provide useful information which isn't revealed by other components of the neurologic examination.
- The presence of a gag reflex does not indicate that the patient is able to protect their airway. Airway protection involves swallowing reflexes, which are far more complex than a simple gag reflex.
- Many people normally lack a gag reflex. Therefore, absence of a gag reflex isn't necessarily pathological, nor does this reveal any definitive information.
- Gagging patients may induce emesis, which could lead to aspiration.
- Further discussion of why gagging patients should be abandoned is here.
(One exception is that among patients with known posterior circulation strokes, serial evaluation of the gag reflex might help track the evolution of brainstem function over time.)
neuroanatomy
- CN11 is a motor nerve that innervates the trapezius (which raises the shoulder) and the sternocleidomastoid muscles. Contraction of one sternocleidomastoid turns the head, whereas contraction of both is involved in head flexion.
- Unilateral upper motor neuron lesion in the cortex causes contralateral weakness of the trapezius, with relative sparing of sternocleidomastoid strength. Similar to the upper facial muscles, the sternocleidomastoid muscle is controlled by the bilateral cerebral hemispheres.(Blumenfeld 2022) However, a focal seizure tends to cause contralateral neck flexion, suggesting that dominant control of each sternocleidomastoid muscle comes from the ipsilateral cerebral hemisphere.
clinical examination
- Trapezius strength is assessed by asking the patient to shrug their shoulders.
- Sternocleidomastoid strength may be assessed by asking the patient to turn their head in both directions. For a supine patient, lifting their head off the pillow requires the bilateral sternocleidomastoid muscles.
neck flexion weakness
- Bilateral weakness of the sternocleidomastoid muscles causes weakness of head flexion (e.g., patient may be unable to lift their head off the pillow).
- Common causes include myasthenia gravis, myopathy, and Guillain-Barre syndrome.
- Weakness of neck flexion may tend to track with respiratory muscle weakness. This could reflect that they share the same segmental innervation.(35863882)
clinical examination
- Dysfunction of CN12-hypoglossal causes the tongue will deviate towards the paretic side.
causes of CN12 dysfunction include:
- Internal carotid dissection.
- Medial medullary syndrome (Dejerine syndrome). 📖
corticospinal tract (aka pyramidal system)
- Upper motor neuron cell bodies lie in the motor cortex (within the precentral gyrus).
- Their axons travel in the subcortical white matter within the posterior limb of the internal capsule.
- They run through the cerebral peduncles into the ventral/anterior brainstem.
- They cross (decussate) at the junction of the medulla and the cervical spinal cord.
- They run down the posterolateral spinal cord.
- Finally, upper motor neuron axons synapse onto lower motor nerves within the anterior horn of the spinal cord grey matter.
more on localization of weakness here: 📖
evaluation of reflexes:
- Standard numeric scale:
- 0 = Absent.
- 1+ = Reduced, or seen only on reinforcement.
- 2+ = Normal.
- 3+ = Brisk.
- 4+ = Hyperreflexia associated with unsustained clonus.
- 5+ = Hyperreflexia with sustained clonus.
- 💡 Deep tendon reflexes are normal if they are 1+, 2+, or 3+ as long as they are symmetric and there isn't a dramatic difference between arms versus legs.(Blumenfeld 2022)
- Spreading of reflexes to muscles that aren't being tested is a reflection of hyperreflexia.
neuroanatomy of commonly tested reflexes:
- Biceps: C5-C6.
- Brachioradialis: C6.
- Triceps: C7.
- Patellar: L4.
- Achilles: S1.
For supine patients, patellar and ankle reflexes require supporting the joint in a mildly flexed position, as shown below. Crossing the patient's legs at the shins may also be helpful. A video on reflex testing is here.
general comments
- Clonus may be conceptualized as a form of profound hyperreflexia, wherein each muscle contraction triggers another reflexive contraction.
- Nonsustained clonus (<5-10 beats) that is symmetric may be normal. However, sustained clonus (>5-10 beats) is always abnormal.(30521283) Unfortunately there is some confusion about how to define “sustained clonus,” with some authors using this to refer to clonus that occurs indefinitely.(33522735)
- As part of the physical examination, ankle clonus is generally tested (video below). However, clonus may occur at other joints as well (e.g., it could be inadvertently triggered while testing a patellar reflex).
- Spontaneous clonus is triggered by minor movement, leading to rhythmic, large muscle contractions. This may be confused with seizures.
- 🎥: Clonus
causes of clonus include:
- Upper motor neuron dysfunction as spasticity develops (e.g., due to stroke, trauma, cerebral palsy, or multiple sclerosis).
- Toxicological:
- 💡 Toxicological clonus may be suggested by symmetric clonus and diffuse hyperreflexia (without any focal neurological signs).
- Serotonin syndrome 📖 is the most common toxicological association. Clonus due to serotonin syndrome is usually most prominent in the legs.
- Anticholinergic toxicity.
- Baclofen withdrawal.
- Other:
how to evaluate
- The patient's leg should be extended at the knee.
- Firm pressure with a somewhat sharp object should be applied to the lateral portion of the sole of the foot near the heel and slowly moved upwards. If there is no response, the stimulus can be turned when it reaches the base of the fifth toe and continued medially towards the ball of the foot.(Alpert 2019)
- The initial movement of the large toe determines the reflex.
- Flexion (downward movement) is normal.
- Upwards (extension) movement is abnormal, termed a “positive Babinski sign.”
- It may sometimes to difficult to sort out a withdrawal response versus a Babinski sign. The Chaddock maneuver may also be used to elicit the same reflex, but this is less likely to elicit a withdrawal response.(Alpert 2019)
- A video showing evaluation of the Babinski sign.
significance
- A Babinski sign (upward extension of the large toe) is always abnormal [in adults]. This is an indication of upper motor neuron disease.
- A unilateral Babinski sign indicates pathology somewhere within the corticospinal tract (contralateral cerebral hemisphere, contralateral brainstem, or ipsilateral spinal cord).
- A bilateral Babinski sign:
- In isolation, this often suggests spinal cord pathology.
- A bilateral Babinski sign may result from brainstem or cerebral hemisphere dysfunction (e.g., due to bilateral brain injury, general anesthesia, coma from organ failure, or seizure).(Wijdicks 2021)
- Babinski sign may develop quickly (including even within the postictal phase after a seizure).(18674480)
definition
- Flicking the third digit causes flexion of the first and second digits.
- 🎥: Hoffman's sign.
significance
- The Hoffman sign is generally indicative of an upper motor neuron lesion (e.g., a cervical myelopathy).
- If the Hoffman sign is positive in both hands symmetrically, this may be a normal variant.(Albert 2019)
🎥: How to evaluate muscle tone
causes of increased motor tone or rigidity
- Intoxication (e.g., serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia).
- Withdrawal of Parkinson's medications.📖
- Seizure.
- Upper motor neuron lesion (involving the corticospinal tract).
- Basal ganglia dysfunction.
- Bilateral frontal lobe dysfunction may cause paratonic rigidity (discussed further below).
causes of flaccidity
- Acute upper motor neuron lesion (especially spinal cord injury) – may initially cause flaccidity, before development of spasticity. This may occur in the context of spinal shock.📖
- Lower motor neuron lesion.
- Intoxication.
- Chemical paralysis.
multifocal myoclonus –more on this here 📖
asterixis (negative myoclonus)
definition
- Asterixis refers to sudden, brief, arrhythmic lapses of sustained posture due to involuntary interruption in muscle contraction.(27807107)
- This is commonly assessed by asking the patients to hold their hands outstretched, as if they were stopping traffic. Asterixis may begin after a latent period of 30 seconds, so be cautious about immediately concluding that there is no asterixis.(27807107)
- Asterixis is usually an asymptomatic examination finding, but it can cause symptoms.
causes include
- Metabolic derangements:
- Hepatic encephalopathy (although asterixis may be lost in the most severe stages of hepatic encephalopathy).
- Uremic encephalopathy.
- Hypercapnia and/or hypoxemia.
- Hypoglycemia.
- Severe electrolyte abnormalities (hypokalemia, hypomagnesemia).(36625084)
- Urea cycle defects causing hyperammonemia.
- Wilson's disease.
- Medication:
- Antiseizure medications (e.g., phenytoin, valproate, carbamazepine, gabapentin).
- Levodopa.
- Opioids.
- Anticholinergics.
- Benzodiazepines.
- Lithium.
- Clozapine.
- Structural lesions (often involving the thalamus):(27807107)
- Hemorrhage (subdural, subarachnoid, or intraparenchymal).
- Infarction.
- Neoplasia (primary or metastatic).
- Cerebral toxoplasmosis.
- Viral encephalitis.
fasciculations
- Fasciculations are small involuntary muscle contractions that don't cause movement across a joint.
- Causes of fasciculations:(27907965)
- Any disease involving the lower motor neurons.
- Electrolyte abnormalities (e.g., hypomagnesemia, hypokalemia).
- Hyperthyroidism.
- Medication side effect (e.g., steroid, acetylcholinesterase inhibitors, isoniazid, bronchodilators, caffeine).
- Benzodiazepine withdrawal.
- Uremia.
- Following brain death.
tremor: more common causes in the ICU
- Structural lesions:
- Cerebellar lesion (intention tremor).
- Midbrain lesion (postural tremor).
- Medication-induced:
- Beta-agonists.
- Dopamine antagonists.
- Valproate.
- Amiodarone.
- Cyclosporine, Tacrolimus.
- Lithium 📖.
- Withdrawal (e.g., alcohol or opioid).(Wijdicks 2021)
- (Tremors may occur as a component of acute onset parkinsonism, discussed further here: 📖)
paratonic rigidity (gegenhalten)
- Paratonic rigidity is a form of hypertonia marked by involuntary variable resistance to passive movements (especially a quick movement of the arm). Resistance occurs with a force equal and opposite to that applied by the examiner. This may be misinterpreted as oppositional behavior.(Alpert 2019)
- Causes:
- Frontal lobe disorders, especially bilateral frontal lobe dysfunction (may be accompanied by a grasp reflex).(Louis 2021)
- Metabolic encephalopathy.
- Catatonia. 📖
Gait often cannot be tested in critically ill patients, but extremity coordination may be tested as follows (video here):
- Finger-nose-finger test.
- Rapid alternating movements (dysdiadochokinesia).
differential diagnosis of discoordination
- Contrary to popular belief, poor performance on the above tests doesn't necessarily indicate a cerebellar lesion. Instead, it may reflect a pathology involving the cerebellum, proprioception, vision, basal ganglia, or motor pathways.
- Cerebellar pathology is likely only if abnormalities in other subsystems have been excluded (e.g., adequate vision, intact strength, normal reflexes, intact proprioception, and absence of other features of basal ganglia dysfunction).
neuroanatomy of vibration & proprioception: posterior (dorsal) column – medial lemniscus pathway
- After traveling up the dorsal column of the spinal cord, axons ascend to the posterior column nuclei in the medulla:
- Nucleus gracilis (from the lower body; more medial).
- Nucleus cuneatus (from the upper body; more lateral).
- Neurons from these nuclei decussate in the base of the medulla (similarly to the corticospinal tract), subsequently forming the medial lemniscus.
- The medial lemniscus travels to the VPL (ventral posterior lateral) nucleus of the thalamus, which is also the destination of the anteriolateral (spinothalamic) tract.
- Finally, neurons project through the posterior limb of the internal capsule to the primary somatosensory cortex.
evaluation: vibration sense
- Start by stimulating the pulp of digits (e.g., toes or fingers). If this isn't sensed, then stimulate more proximally until the patient is able to perceive vibration. Avoid stimulation over bones, as the bone may transmit vibration proximally.
- Ideally this is performed with a tuning fork (preferably a 128-Hz or 64-Hz tuning fork, but 256-Hz may also be adequate).(Blumenfeld 2022) However, a tuning fork is often unavailable.
- Smartphone applications may be used to provide these frequencies (e.g., a free iphone app onsA440 allows for production of a 128-Hz sound that generates perceptible vibration if the phone speaker is gently held to the skin). To avoid cross-contamination, cover the phone with a clear plastic bag before contacting the patient. Vibration may not be effectively transmitted unless the speaker is held fully over the skin. The examiner may touch the patient's skin next to the phone to confirm that vibration is being effectively transmitted to the patient.
evaluation: position sense
- Position sense may be evaluated by determining if the patient can sense very subtle adjustments to finger or toe position, either upwards or downwards. The digit should be gently grasped from the sides, to avoid providing tactile clues regarding which direction the digit is being moved (video here). Only small movements are necessary, as normal perception should allow for the detection of movements which are barely perceptible to the eye.(Blumenfeld 2022)
neuroanatomy of pain and temperature: anterolateral (spinothalamic) tract
- Unlike the other major tracts, the dorsal root neurons decussate immediately within the spinal cord. Subsequently, second-order neurons ascend within the anterolateral spinal cord.
- It takes 2-3 spinal segments for the fibers to reach the opposite side of the spinal cord. Thus, a lateral cord lesion will affect contralateral pain sensation beginning a few segments below the level of the lesion.(Blumenfeld 2022)
- Eventually, these neurons join the medial lemniscus in the pons and travel together with the dorsal column neurons to the ventral posterolateral nucleus of the thalamus.
- Clinically, pain perception can be measured by determining whether a pin is perceived as feeling sharp.
evaluation
- Temperature may be evaluated by asking the patient to close their eyes and then touching the skin with either a plastic cup of ice water or a cup of warm water (items easily obtainable in an ICU). Another technique is wiping the skin with an alcohol prep pad, which generates a cool patch of skin due to evaporative cooling – this should generally be perceived as being cold.(25340491)
- Pain sensation may be evaluated by determining whether the patient can perceive a gentle stimulation from a pin or broken wooden swab as “sharp” (video here). The skin should be stimulated very gently and not broken. Nonetheless, a clean pin should be used for each patient and disposed of subsequently.
monocular vision loss
- Pathology before the optic chiasm:
- Ocular problem:
- Lens (e.g., cataract).
- Anterior chamber (e.g., uveitis).
- Retina (e.g., retinal ischemia).
- Optic nerve problem (e.g., optic neuropathy).
- Ocular problem:
bitemporal hemianopsia
- Pathology at the optic chiasm.
- Causes:
- Often due to pituitary lesions.
- Sellar meningioma or craniopharyngioma.
- Aneurysm of the distal carotid.
homonymous hemianopsia
- One study involving 904 patients found the following lesions among patients with homonymous hemianopsia: (16567710)
- Occipital lobe (45%).
- Optic radiations (32%).
- Optic tracts (10%).
- Lateral geniculate body of the thalamus (1%).
homonymous quadrantanopia
- Generally localizes to the optic radiation or the occipital lobe.
cortical blindness
- Severe, bilateral occipital lobe damage may cause the brain to be unable to understand visual information. This can be caused by bilateral PCA (posterior cerebral artery) strokes.
- Anton syndrome: Patient is unaware that they are blind.
- Charles Bonnet syndrome: Release hallucinations occur, often involving small people. The patient generally knows that these are not real.
Neglect may often be evaluated during other components of the neurological examination (e.g., while testing for facial sensation to evaluate the trigeminal nerve).
evaluation of neglect
- Sensory neglect:
- Simultaneous stimulation on both sides of the body may be recognized only on one side (extinction on double simultaneous stimulation). This is easily tested when examining skin sensation (cranial nerve V) or testing visual fields.
- Patients may ignore half of the room (e.g., paying attention to the examiner only if approached from the patient's right side).
- Motor neglect:
- The neglected side has intact strength, but is moved only if attention is strongly directed towards it.(Blumenfeld 2022)
- During strength testing, if asked to perform a motor task bilaterally (e.g. “step down on the gas”), the patient may perform the task only unilaterally.
- Constructional neglect: If asked to draw a clock, half of the clock may be ignored.
causes of neglect
- Obvert neglect usually reflects right parietal lobe dysfunction, causing left-sided neglect. However, this may also result from right frontal lesions, right thalamic or basal ganglia lesions, or rarely right midbrain lesions.(Blumenfeld 2022)
- Left parietal lobe dysfunction can cause right-sided neglect, but this is usually more subtle.
Below are some general rules of thumb. Please note that they are not uniformly valid (for example, in a patient with numerous distributed lesions).
loss of specific sensory modes
- The dorsal columns and spinothalamic tracts merge together in the lower medulla.
- Selective loss of some modes of sensation (e.g., vibration but not pain) indicates a lesion below the lower medulla.
- Loss of all modes of sensation may indicate either:
- a lesion above the lower medulla.
- a lesion in the spinal cord involving all tracts.
facial involvement
- (+) Facial involvement (either sensory or motor) requires a lesion in the brainstem or higher up in the neuraxis (not the spinal cord).
isolated bilateral motor loss, or isolated bilateral sensory loss
- This generally suggests a lesion in the spinal cord, or in the peripheral nerves (or the neuromuscular junction or muscle, in the case of weakness).
- Bilateral findings imply bilateral lesions, which will generally cause some other abnormality.
- An exception is that a medial lesion affecting the bilateral leg areas of the motor cortices may cause paraplegia and incontinence mimicking a spinal cord lesion. This can result from bilateral anterior cerebral artery infarction or a tumor near the midline. However, this lesion will typically also cause cognitive deficits (more on anterior cerebral infarction: 📖).
frontal lobe
- Left frontal lobe:
- Broca's area lies in the inferior frontal gyrus. Damage may cause a nonfluent aphasia with preserved comprehension. Broca's area may sometimes lie on the right side in left-handed patients.
- Poor executive function, abulia (apathy).(27907952) Damage may cause behavioral disinhibition.
- Frontal eye fields:
- Activation of the frontal eye fields drives the eyes to look towards the contralateral side.
- Seizure involving the frontal lobe will activate the frontal eye fields, causing the eyes to deviate away from the lesion (looking towards the shaking extremity).
- Stroke involving the frontal lobe will inactivate the frontal eye fields, causing the eyes to deviate towards the lesion (looking away from the paretic extremity).
- Dorsolateral prefrontal cortex (disorganized):
- Perseveration.
- Impaired digit span.
- Mesial frontal lobe (akinetic-mute): minimal spontaneous action/speech.
- Orbitofrontal cortex (disinhibited):
- Impulsive, emotionally labile.
- Inappropriate jocularity.
- Hypersexuality.
temporal lobe
- Lesions in the medial temporal lobes (including the hippocampus) cause amnesia. This is especially problematic if the dominant hippocampus is damaged.
- The superior temporal gyrus of the temporal lobe is the primary auditory cortex, involved in processing sounds.
- Right temporal lobe – music-melody perception (27907952)
- Left temporal lobe: Wernicke's area is located in the posterior temporal gyrus. Damage may cause a receptive aphasia that results in fluent production of nonsensical speech.
- Damage to the Meyer loop visual fibers could cause a superior quadrantanopia.
- Apathy may result from left temporal injury.(27907952)
parietal lobe: Spatial attention and praxis
- Spatial attention & neglect:
- The parietal lobe combines information from the somatosensory cortex and the visual cortex to determine where objects are in space.
- Lesions cause neglect: objects in half of space fall off the patient's radar.
- Neglect is more common in lesions of the nondominant parietal lobe (usually a right-sided parietal lobe causing left-sided neglect). This may cause anosognosia – patients are unaware of neurologic deficits.
- Mathematical processing:
- Predominantly occurs in the dominant parietal lobe.
- Lesions in the angular gyrus of the dominant hemisphere can cause Gerstmann's syndrome: Left-right confusion, inability to count (acalculia), inability to name fingers (finger agnosia), and inability to write (agraphia).
- Apraxia:
- Dominant parietal lobe lesions may cause apraxia bilaterally. (Praxis begins in the left parietal lobe, and then information is sent to the bilateral prefrontal motor areas, which each direct praxis on the contralateral side of the body.).
- Eyelid opening apraxia is discussed above.📖
- Balint's syndrome may occur due to bilateral parietal lobe lesions:
- (1) Simultanagnosia – inability to perceive global elements. Patients have problems with visuospatial attention.
- (2) Optic ataxia: Difficulty with finger-nose movements because patients cannot locate elements in space. There is poor reaching under visual guidance (yet intact ability to return the finger to the nose).
- (3) Ocular apraxia (inaccurate saccades).
occipital lobe
- Either occipital lobe may cause a visual field cut.
- Visual information flows from the occipital association cortex to the temporal lobe in the “what” pathway. (figure above) Different hemispheres vary in the type of information they process:
- Left “what” pathway of the occipital & nearby temporal lobe:
- The left side of the brain is generally involved in language.
- Lesions in the left occipital association cortex may cause alexia without agraphia. 📖
- Right “what” pathway of the occipital & nearby temporal lobe impairs facial recognition. Damage may cause prosopagnosia (inability to recognize people).
- Left “what” pathway of the occipital & nearby temporal lobe:
Some generalizations may be helpful in lesion localization:
(#1/3) vertical localization within brainstem
- Midbrain: CN 2-4 (pupils, vertical eye movements).
- Pons: CN 5-8 (vestibular, horizontal eye movements, facial weakness).
- Medulla: CN9-12 (tongue, larynx).
(#2/3) anterior (ventral) vs. posterior (dorsal)
- Anterior lesion: Corticospinal tract.
- Posterior lesion:
- Cerebellar peduncles (causes ipsilateral ataxia).
- Sensory function of cranial nerves.
- Lesion in a cranial nerve nucleus (e.g., nuclear CN3 palsy 📖).
(#3/3) medial vs. lateral
- Medial:
- Motor nuclei of cranial nerves.
- Corticospinal tract (motor pathway).
- MLF (medial longitudinal fasciculus).
- Causes INO (internuclear ophthalmoplegia). 📖
- Lesion is ipsilateral to the eye that cannot adduct.
- Medial lemniscus (vibration/proprioception).
- Lateral:
- Descending sympathetics (ipsilateral Horner's syndrome).
- Spinothalamic tract (ascending pain/temperature).
- Sensory nuclei of CN5-trigeminal (facial sensation).
- Spinocerebellar tract (ipsilateral ataxia).
unilateral ventral (anterior) midbrain peduncle = Weber syndrome
- Clinical findings:
- (1) Ipsilateral CN3 palsy due to involvement of the CN3 fascicle.
- (2) Contralateral hemibody weakness (corticospinal tract).
- May be caused by occlusion of the paramedian branches at the top of the basilar artery.
unilateral dorsomedial midbrain (Claude syndrome)
- (1) Ipsilateral CN3 palsy (fascicle of CN3).
- (2) Contralateral tremor and ataxia (red nucleus & cerebellothalamic fibers).
unilateral paramedian midbrain (Benedikt syndrome)
- This is a combination of Weber and Claude syndromes, due to infarction of an area overlapping both regions.
- (1) Ipsilateral CN3 palsy (fascicle of CN3).
- (2) Contralateral hemibody weakness (cerebral peduncle).
- (3) Contralateral tremor and ataxia (red nucleus & cerebellothalamic fibers).
- (4) May have contralateral rigidity (substantia nigra).
bilateral ventral (anterior) midbrain (27907952)
- Abnormal consciousness or agitated delirium (reticular activating system).
- Vertical gaze palsy (colliculi).
- Miosis (sympathetic nerve).
dorsal midbrain syndrome (aka Parinaud syndrome, pretectal syndrome, Sylvian aqueduct syndrome, posterior commissure syndrome)
- Features include (27907952)
- Impaired upgaze (initially this may be evident only with saccades, but eventually a complete paralysis of upgaze may occur).
- Convergence-retraction nystagmus may be triggered by upward gaze. Simultaneous activation of all extraocular muscles cause retraction of the eyes into the orbit.
- Pupils are usually large and poorly responsive to light, but they do respond to accommodation (“light-near dissociation”).
- Eyelid retraction may occur (Collier's sign).
- Typically localizes to lesions in the midbrain around the cerebral aqueduct and involving the corpora quadrigemina and posterior commissure.(32924623)
- Common causes include:
- Hydrocephalus, particularly fourth ventricular outflow obstruction. 📖
- Tumor (e.g., pineal tumor or tectal glioma).
- Multiple sclerosis.
- Stroke.
- 🎥: Parinaud's syndrome.
lateral mid-pontine syndrome
- Ipsilateral ataxia (due to involvement of middle cerebellar peduncle).
- Contralateral impairment in arm/leg pain and temperature sensation (spinothalamic tract involvement).
- Ipsilateral facial numbness (CN5-trigeminal).
- Ipsilateral paralysis of mastication (motor component of CN5-trigeminal).
inferior lateral pontine syndrome (Marie-Foix syndrome)
- Clinical consequences:
- Ipsilateral ataxia (due to involvement of middle cerebellar peduncle).
- Impairment of pain and temperature sensation in the ipsilateral face (CN5-trigeminal nucleus & tract) and the contralateral arm/leg (spinothalamic tract).
- Ipsilateral Horner's syndrome (descending sympathetic chain).
- Ipsilateral facial paralysis (CN7-facial).
- Vertigo/hearing loss (CN8-vestibulocochlear nerve nucleus or ischemia of the vestibular apparatus/cochlea itself, which is supplied via the AICA).
- Caused by occlusion of the AICA (anterior inferior cerebellar artery).
lateral medullary syndrome (Wallenberg syndrome)
- Clinical consequences:
- Ipsilateral ataxia, vertigo, nystagmus, and nausea (due to involvement of inferior cerebellar peduncle & CN8-vestibular nuclei).
- Impairment of pain and temperature sensation in the ipsilateral face (CN5-trigeminal nucleus & tract) and the contralateral arm/leg (spinothalamic tract).
- Ipsilateral Horner's syndrome (descending sympathetic fibers in lateral medulla).
- Hoarseness and dysphagia (involvement of the nucleus ambiguous, CN10-vagus).
- 🫁 Rarely, may also cause central hypoventilation syndrome with loss of respiratory drive when asleep (aka, Ondine's curse).
- Caused by occlusion of the vertebral artery, or (less commonly) the PICA (posterior inferior cerebellar artery).
medial mid-pontine syndrome
- Contralateral hemibody weakness (corticospinal tracts).
- Contralateral vibration/proprioception loss (medial lemniscus).
- Ipsilateral ataxia (superior cerebellar peduncle).
inferior medial pontine syndrome (Foville syndrome)
- Due to occlusion of basilar perforators (paramedian branches).
- Clinical consequences may include:
- Contralateral hemibody weakness (corticospinal tracts).
- Contralateral vibration/proprioception loss (medial lemniscus).
- Ipsilateral CN7-facial weakness (facial colliculus).
- Ipsilateral conjugate gaze palsy (nucleus of CN6-abducens), possibly accompanied by one-and-a-half syndrome if the MLF (medial longitudinal fasciculus) is also involved.📖
medial medullary syndrome (Dejerine syndrome)
- Clinical consequences:
- Contralateral arm/leg weakness, usually sparing the face (corticospinal tracts).
- Tongue deviation towards the lesion (Ipsilateral CN12-hypoglossal nucleus).
- Contralateral reduced position and vibration sense (medial lemniscus).
- Due to paramedian branches of anterior spinal artery or vertebral artery.
vermis (27907952)
- Ataxia of gait (truncal ataxia, which affects the proximal musculature).
- Hypotonia.
- Nystagmus.
- Dysarthria.
hemisphere (27907952)
- Incoordination and dysmetria (dentate nucleus).
- Appendicular ataxia (affecting the ipsilateral limbs).
- Nystagmus.
- Ataxic speech (may sound drunk).
- The key finding is that brainstem reflexes are usually intact (e.g., pupillary reflexes, corneal reflexes, and vestibulo-ocular reflexes). There are a few exceptions however:
- Very deep intoxication (e.g., barbiturate or baclofen overdose) may cause loss of cranial nerve reflexes.
- Anticholinergic poisoning or anoxic-ischemic injury may cause loss of pupillary reactivity.
- Spontaneous eye movements can occur (e.g., roving conjugate gaze, dipping with slow downgaze followed by rapid upgaze, or ping-pong gaze back and forth).(28187795)
- Upward or downward eye deviation can occur.
- Adventitious limb movements may be seen. If present, multifocal myoclonus, asterixis, or tremor support a metabolic etiology.(28187795) Any motor signs are usually symmetric.
- Gegenhalten (paratonic rigidity) may be seen.(Louis 2021)
clinical findings in uncal herniation
- Ipsilateral blown pupil:
- Initially, the pupil is dilated and sluggish. Parasympathetic fibers run along the outside of CN3-oculomotor, so pupillary dilation can occur first.
- With progression, the pupil becomes fixed and dilated. Impaired consciousness is almost always present by the time the pupil is fixed and dilated.(Nelson, 2020)
- With progression, oculomotor paralysis occurs (causing the eye to be locked in a down-and-out orientation).
- Ipsilateral ptosis results from denervation of the levator palpebrae superioris.(26704760)
- (Further discussion of CN3-oculomotor palsy above 📖).
- Contralateral hemiparesis due to compression of the cerebral pedicle
- Hemiparesis may be accompanied by hyperreflexia and a positive Babinski's sign.
- If untreated, this may eventually compress the midbrain (e.g., causing bilateral fixed & dilated pupils, with decorticate or decerebrate posturing).
Kernohan's notch phenomenon
- Definition: Lateral displacement of the midbrain can compress the contralateral cerebral peduncle. This causes weakness ipsilateral to the herniation (a false localizing sign).
- The CN3-oculomotor palsy sometimes remains correctly localizing (ipsilateral to the herniation). 📄 Thus, Kernohan's notch phenomenon could be suggested by ipsilateral pupillary dilation and weakness.(32938557)
key radiological findings
- The earliest finding may be effacement of the suprasellar cistern.
- Widening of the ipsilateral perimesencephalic cistern (since the midbrain is pushed away from the hernia).
- Hydrocephalus may be seen (especially involving the contralateral lateral ventricle).
anatomy
- Uncal herniation is often the first event in downward transtentorial herniation, followed by herniation of more posteriorly located brain tissue.
- Compression of the PCA (posterior cerebral artery) may cause infarction of the medial temporal and occipital lobe (white arrowhead in the figure above).
- Compression of the aqueduct of Sylvius may cause hydrocephalus.
- Compression of the reticular activating system in the midbrain may cause unconsciousness.
posterior lateral downward transtentorial herniation
- Uncal herniation (discussed above) refers to downward herniation of the anterior portion of the temporal lobe.
- Less commonly, mass lesions located more posteriorly within the head may cause downward herniation of the posterior portion of the temporal lobe. This may cause impingement on the lateral part of the quadrigeminal plate cistern.(31589570)
- Clinical manifestations may include:(31589570)
- Involvement of the tectum at the level of the superior colliculus may cause Parinaud syndrome.
- Compared to uncal herniation, there is less involvement of CN3-oculomotor nerve or the PCA (posterior cerebral artery).
Downward central herniation often occurs in combination with downward lateral herniation.
clinical features
- (1) Diencephalic stage (localized to the thalamus):
- Disruption of the reticular activating system causes drowsiness and confusion.
- Miotic (small) pupils are initially a prominent sign, often with restricted upgaze (Parinaud syndrome). Uncommonly, a unilateral Horner's syndrome may occur early on (before transitioning to bilateral small pupils).(Alpert 2019)
- ⚠️ Initially, this may resemble an intoxication causing small pupils (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors). There may initially be conjugate roving eye movements, simulating a toxic/metabolic coma.
- (2) Midbrain-upper pons stage (mesencephalic stage):(32809371)
- Coma deepens.
- Midbrain dysfunction emerges: pupils may become fixed & mid-position.
- Abnormal motor responses (e.g., posturing) may be an early clue to a structural etiology of the coma. Decorticate and later decerebrate posturing occur, with bilateral extensor Babinski reflexes.
- Pontine dysfunction emerges, with loss of vestibulo-ocular reflexes and corneal reflexes.
- Pathological breathing patterns may emerge (e.g., central neurogenic hyperventilation).
- (3) Medullary stage: (32809371)
- Breathing may slow and become irregular (ataxic breathing).
- Cushing's reflex may occur with hypertension and bradycardia. Pupils may temporarily dilate due to a surge of epinephrine release.
clinical findings
- Vertical gaze palsy may be followed by stupor/coma.(34618757)
- Pupils may be fixed and either midposition or dilated.
- Cerebral aqueduct compression may result in acute hydrocephalus.
- Patients may also have impaired swallowing and aspiration, due to compression of the brainstem.
- Branches of the SCA (superior cerebellar arteries) and the PCA (posterior cerebral arteries) may be compressed, causing infarction of the superior portion of the cerebellar hemisphere and the occipital lobe.(31589570)
causes include
- (1) Mass effect from the posterior cranial fossa, especially a mass originating near the opening of the tentorium cerebelli (e.g., within the cerebellar vermis).
- (2) Sudden relief of supratentorial intracranial hypertension (e.g., due to placement of an external ventricular drain).
radiologic findings
- The quadrigeminal cistern is distorted.
- Compression of the aqueduct of Sylvius may cause hydrocephalus.
clinical findings
- Stiff neck may be a very early sign.(Alpert 2019)
- Cranial nerve palsies and stupor/coma result from brainstem compression.
- Decerebrate posturing may occur initially, but eventually flaccid paralysis occurs.
- Cushing reflex may occur including hypertension, bradycardia, and slow respirations.(34618757) Compression of the medulla may eventually lead to central hypoventilation with respiratory arrest.
neuroanatomy
- Acute hydrocephalus may occur (due to compression of the fourth ventricle). This may accelerate the process of herniation and consciousness impairment.
- Tonsillar herniation may cause infarction of the PICA (posterior inferior cerebellar artery), causing infarction of the cerebellum and lateral medulla.(32924623)
clinical findings
- Contralateral leg weakness is a central finding, due to compression of the ipsilateral anterior cerebral artery. Posturing of the leg may also be seen.
- Mental status is relatively unaffected, as compared to other herniation syndromes. However, there may be apathy and indifference.(31589570)
anatomic considerations
- The cingulate gyrus herniates underneath the falx cerebri. This may eventually cause necrosis of the ipsilateral cingulate gyrus.
- ACA (anterior cerebral artery) infarction may occur.(32924623)
- Falcine herniation may compromise both foramina of Monro, causing dilation of the contralateral ventricle (the ipsilateral ventricle tends to be directly compressed).
- Ultimately, this may progress to central downwards herniation over time (due to increasing edema of herniated tissue).
- Cranial nerves:
- Pupillary reflexes are often intact (since these are located in the midbrain, which is above the level of compression).
- Absent corneal reflexes and abnormal vestibulo-ocular reflexes are often seen. Skew deviation may occur (one eye looks up, the other looks down).
- Ocular bobbing can occur, or nystagmus that may be direction-changing or vertical.(28187795)
- Extensor or flexor posturing can occur.
To keep this page small and fast, questions & discussion about this post can be found on another page here.
Acknowledgement: Thanks to Dr. Casey Albin (@caseyalbin) for thoughtful comments on this chapter.
Guide to emoji hyperlinks 
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