Cranial nerves. Intracranial hypertension.
Consciousness disturbances. Vertebral
column examination.
Jan Kolcava
Cranial nerves
Cranial nerves
• I. Olfactory nerve
• II. Optic nerve
• III. Oculomotor nerve
• IV. Trochlear nerve
• V. Trigeminal nerve
• VI. Abducens nerve
• VII. Facial nerve
• VIII. Vestibulocochlear nerve
• IX. Glossopharyngeal nerve
• X. Vagus nerve
• XI. Accessory nerve
• XII. Hypoglossal nerve
Teachmeanatomy.info
Cranial nerves – part I
• The olfactory nerve (I): The sense of smell.
• The optic nerve (II): This nerve carries visual information from the retina of the eye to the
brain.
• The oculomotor nerve (III): The nerve controls most of the eye’s movements, the
constriction of the pupil, and maintains an open eyelid.
• The trochlear nerve (IV): A motor nerve that innervates the superior oblique muscle of
the eye.
• The trigeminal nerve (V): This is responsible for sensation in the face and motor function
of the mouth.
• The abducens nerve (VI): A motor nerve that innervates the lateral rectus muscle of the
eye.
Cranial nerves – part II
• The facial nerve (VII): Controls the muscles of facial expression, and functions in the conveyance of taste sensations
from the anterior two-thirds of the tongue.
• The vestibulocochlear nerve (VIII): Responsible for transmitting sound and balance information from the inner ear
to the brain.
• The glossopharyngeal nerve (IX): This nerve receives sensory information from the tonsils, the pharynx, the middle
ear, and the rest of the tongue.
• The vagus nerve (X): The nerve is responsible for many tasks, including heart rate, gastrointestinal peristalsis,
sweating, and muscle movements in the mouth.
• The spinal accessory (XI): Innervation of trapezius and sternocleidomastoideus muscles.
• The hypoglossal nerve (XII): This nerve controls the tongue movements of speech, food manipulation, and
swallowing.
• * There are many mnemonic devices to remember the cranial nerves („Ooh, Ooh, Ooh To Touch And Feel Very Good
Velvet. Such heaven!“…).
Olfactory nerve (I) -
anatomy
• The olfactory nerve relays smell information to the
cortex via a three-neuron pathway.
• First-order sensory neurons are located in the mucosa of the
upper nasal septum and superior nasal concha. These bipolar
neurons bundles collectively called the olfactory nerves. The thin,
unmyelinated olfactory fibers enter the anterior cranial fossa via
the cribriform plate of the ethmoid bone.
• Second-order sensory neurons are located in the olfactory bulb.
Their axons course in the olfactory tract to the medial or lateral
olfactory striae. These axons synapse in the amygdala, the
prepiriform area, or neighboring areas.
• Third-order neurons relay the information to the cerebral cortex.
Journal de Radiologie Diagnostique et Interventionnelle, Volume 94, Issue 10, October 2013, Pages 992-999.
Studyblue.com
Olfactory nerve (I) - examination
• The olfactory nerve mediates the sense of smell (olfaction).
• Gross assessment: ask the patient about the ability to smell and changes of food flavor
• More detailled testing: With eyes closed, ask the patient to sniff a mild stimulus such as
toothpaste,coffee, cloves or soap and identify the odorant. Each nostril is tested separately.
• Irritants such as alcohol should not be used because they may be detected as noxious stimuli
independent of olfactory receptors.
• Pathology: hyposmia x anosmia x dysosmia;
• smell pseudohallucination – epileptic seizure affecting uncus gyri hippocampi
• *Testing is usually omitted unless there is suspicion for inferior frontal lobe disease, in persons who
experience spontaneous loss of smell, in patients with a Parkinson's disease, and patients who
have suffered head injury.
Optic nerve (II)-
anatomy
• The optic nerve relays sight information from the retina to
the visual cortex via a four-neuron pathway.
• First-order neurons (rods and cones) in the retina translate
incoming photons into impulses, which are relayed to
second-order bipolar neurons and third-order ganglion cells.
• These retinal ganglion cells combine to form the optic
nerve.
• The optic nerve passes from the orbit into the middle
cranial fossa via the optic canal.
• Ninety percent of the third-order neurons in the optic nerve
synapse in the lateral geniculate body, which then projects
to the cortex.
• Ten percent of the third-order neurons synapse in the
mesencephalon.
• Lesion of the optic nerve may cause partial or complete
loss of vision, depending on the point at which the nerve
is disrupted.
Theodora.com
Optic nerve (II) -
examination
• Check visual acuity (with eyeglasses or contact lens
correction) using a Snellen chart or similar tool.
• Test the visual fields by comparing the patient’s visual
fields to your own.
• Individual eye fields should be tested.
• Face the patient at a distance of approximately 1 m
and place your hands at the periphery of your
visual fields in the plane that is same distance
between you and the patient.
• Instruct the patient to look directly at the center of
your face and to indicate when and where he sees
one of your fingers moving.
• Beginning with the two inferior quadrants and then
the two superior quadrants, observe whether the
patient detects the movements.
Clinicalexams.co.uk; teachmesurgery.com
Optic nerve (II) - examination
• Detailled examination:
• Optic fundi examined with an ophthalmoscope - the color,
size, and degree of swelling or elevation of the optic disc
noted, as well as the color and texture of the retina.
• Detalied perimeter (visual fields) examination.
• VEP – visual evoked potentials
• Pathology:
• Amaurosis
• Visual scotoma
• Hemianopsia (homonymous x heteronymous)
• Cortical blindness
• Visual hallucinations
Morancoreutah.edu.com; en.wikipedia.com
Cranial nerves – oculomotor (III),
trochlear (IV), abducens (VI) -
anatomy
• The oculomotor nerve (CN III) innervates fiive skeletal
muscles in the orbit and parasympathetic
preganglionic fibers from the accessory oculomotor
(Edinger-Westphal) nucleus.
• Postganglionic parasympathetic fibers then course
via short ciliary nerves to the eyeball (these
postganglionic ibers mediate pupillary constriction
and accommodation).
• The trochlear nerve (CN IV) innervates the superior
oblique muscle.
• The abducens nerve (CN VI) innervates the lateral
rectus muscle
healthfavo.com
Cranial nerves – oculomotor (III),
trochlear (IV), abducens (VI) -
examination
• Describe the size and shape of pupils and reaction to light and
accommodation (i.e., as the eyes converge while following
your finger as it moves toward the bridge of the nose).
• To check extraocular movements, ask the patient to keep his
head still while tracking the movement of the tip of your
finger.
• Move the target slowly in the horizontal and vertical planes; observe any
paresis, nystagmus, or abnormalities of smooth pursuit (saccades,
oculomotor ataxia, etc.).
• Ask the patient about diplopia in any direction of gaze; true
diplopia should almost always resolve with one eye closed.
• Horizontal nystagmus is best assessed at 45° and not at
extreme lateral gaze (which is uncomfortable for the patient);
the target must often be held at the lateral position for at
least a few seconds to detect an abnormality.
Ophtobook.com; psychology.wikia.org; allmedtest.com
Cranial nerves – oculomotor (III),
trochlear (IV), abducens (VI) -
examination
• Horizontal and vertical eye movements (full range /
limitations)
• Position of the ocular bulbi:
• parallel, squint (= strabismus – convergent, divergent)
• Presence of nystagmus or other ocular oscillations
• Nystagmus: direction, degree, amplitude, frequency
• Pupil size (normal – midposition, miotic, mydriatic)
• Pupil symmetry (isocoria, anisocoria)
• Pupil shape (round, irregular)
• Pupillary response to light
• direct (illuminated pupil)
• indirect (consesual)
• Ability of convergence and pupilary reaction to it
• (constriction)
http://ophthalmology.stanford.edu/; scielo.br
Cranial nerves – trigeminal
nerve (V)- anatomy
• The major sensory nerve of the head, conveys general somatic
aferents centrally to the trigeminal sensory ganglion (also called
the semilunar or gasserian ganglion) via its ophthalmic (V1),
maxillary (V2), and mandibular (V3) divisions.
• Its mandibular division also innervates skeletal muscles
(masticatory muscles).
• Because of the extensive distribution of CN V, most of the
parasympathetic fibers from CN III, VII, and IX course with
branches of CN V to reach their targets (smooth muscle and
glands) these targets include Lacrimal gland, Submandibular and
sublingual salivary glands, Nasal glands.
• V3 travels to the anterior 2/3 of the tongue, but this sensory input
is not received by trigeminal nuclei but rather by the Solitary
Nucleus.
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
Cranial nerves – trigeminal
nerve (V)- examination
Pinprick and touch sensation on face
• pressure to points where the 3 divisions emerge from the
bone (incisura supraorbitale; froamen infraorbitale;
foramen mentale)- painful?
• Examination of superfitial sensation
• motor part – chewing muscles motorics and strenght
• Reflexes:
• Corneal reflex (touch conjunctiva – blinking)
• Nasopalpebral: blinking after tapping on glabela
• Masseter (jaw-jerk reflex): The mandible is tapped at a
downward angle just below the lips at the chin while the
mouth is held slightly open. In response, the masseter
muscles will jerk the mandible upwards.
• Pathology: positive and negative sensory symptoms
(trigeminal neuralgia).
http://portal.neurocirurgia.org.br/
facial nerve (VII) -
anatomy
• The major motor nerve of the head - somatic
eferents to skeletal muscles.
• Additionally, sends preganglionic
parasympathetic fibers from the superior
salivatory nucleus to the pterygopalatine
ganglia.
• The facial nerve also conveys special visceral
aferents from taste receptors on the anterior
two thirds of the tongue along the chorda
tympani to the geniculate sensory ganglion.
http://impremedia.net/
Facial nerve – central vs. periferal palsy
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.; lookfordiagnosis.com
facial nerve (VII) -
examination
• Look for facial asymmetry at rest and with
spontaneous movements.
• Test eyebrow elevation, forehead wrinkling, eye
closure, smiling, and cheek puff.
• Look in particular for differences in the lower
versus upper facial muscles
• weakness of the lower two-thirds of the face with
preservation of the upper third suggests an upper
motor neuron lesion, whereas weakness of an entire
side suggests a lower motor neuron lesion
• Ask about taste - on the anterior two thirds of the
tongue.
• Hyperacusis – due to a stapiedius nerve laesion.
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
EXAMINATION OF CRANIAL NERVES
–VIII – vestibulocochlear nerve -
anatomy
• Two branches: vestibular (balance) and cochlear (acustic) nerve
• cochlear nerve
• 1. neuron – bipolar cells in ganglion spirale Corti travels via
meatus acusticus internus and pontocerebellar angle to
brainstam
• 2. neuron – auditory nucleii in brainstem (pons) travels as
lemniscus lateralis to colliculi inferiores and corpus
geniculatum mediale (3. neuron) than to cortical area 41
and 42
• vestibular nerve
• 1. neuron - specific sensory cells in semicircular canals and
maculae of the saccule and utricle travels via meatus
acusticus internus and pontocerebellar angle to brainstam
(pons)
• 2. neuron – connected to cerebellum and ocular movement
system; travels to vestibulospinal tract and cortex
http://meduniver.com/
VIII – vestibulocochlear nerve –
examination – cochlear nerve
• Check the patient’s ability to hear a finger rub or
whispered voice with each ear.
• Further testing for air versus mastoid bone
conduction (Rinne) and lateralization of a 512-Hz
tuning fork placed at the center of the forehead
(Weber) should be done if an abnormality is
detected by history or examination.
• Any suspected problem should be followed up
with formal audiometry.
• Ask for tinnitus („perception of sound in
proximity to the head in the absence of an
external source“).
• Pathology: hypacusis/anacusis; tinnitus
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
VIII – vestibulocochlear nerve – examination –
vestibular nerve
• Problems with balance? Vertigo?
• Hautant test: The patient is seated. The examiner stands close to the patient. The patient
flexes both arms to 90 with forearms supinated. The patient is instructed to close their
eyes – examiner observes drifting of one of the arms.
• Romberg test:
• I = the subject to stand up
• II = the subject stands with feet together, eyes open
• III = the subject stands with feet together and closes the eyes
• IV + V = III + head to the right/left sice
• Gait: normal + eyes closed
Phzsio-pedia.com
VIII – vestibulocochlear nerve –
examination – vestibular nerve
• Vertigo + vomiting
• Nystagmus
• Involuntary eye movement, acquired in infancy or later in
life, that may result in reduced or limited vision
• Horizontal x vertical x rotatoric
• Direction - named according to quick component of
nystagmus (but the pathogenic is the slow component of
nystagmus)
• Intensitiy
• I. Degree - moderate lateral gaze
• II. Degree - spontaneous on forward gaze
• III. Degree – forvard and both sides
• Speed (slow x fast)
• Amplitude (fine x coarse)
http://resumepedia.us/; http://commons.wikimedia.org/
VIII – vestibulocochlear nerve –
examination – vestibular nerve
syndromes
• Peripheral vestibular dysfunction
• Result from any lesion affecting the vestibular nerve,
the receptors, or the structures that house the
receptors. Clinical signs may consist of vestibular
ataxia, ipsilateral Hautant/Romberg, and nystagmus
in the direction away from the lesion.
• Usually last no longer than one week.
• Central vestibular dysfunction
• Central vestibular dysfunction may look peripheral,
but peripheral vestibular dysfunction will never look
central.
• May include vertical nystagmus or nystagmus that
changes direction, a Hautant/Romberg test can be
towards or away from the lesion.
EXAMINATION OF
CRANIAL NERVES – IX-X
• The glossopharyngeal nerve (IX) innervates the muscles from the
third embryonic branchial arch and sends preganglionic
parasympathetics from the inferior salivatory nucleus via the
lesser petrosal nerve to the otic ganglion.
• The vagus nerve (X) innervates the pharyngeal and laryngeal
muscles of the fourth embryonic branchial arch and sends
preganglionic parasympathetic fibers from its dorsal nucleus to
smooth muscle and glands of the neck, thorax (including cardiac
muscle of the heart), and proximal two thirds of the abdominal GI
tract.
• Vagal aferents arise from visceral structures of the same
thoracic and GI regions and from aortic baroreceptors and
chemoreceptors that course to the brainstem. Special
sensory fibers from taste buds on the epiglottis and general
somatic aferents arising from skin around the ear, larynx,
external acoustic meatus, and posterior dura mater also
travel in the vagus nerve.
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
EXAMINATION OF
CRANIAL NERVES – IX-X
• Observe the position and symmetry of the palate and uvula at rest
and with phonation (“aah”).
• The pharyngeal (“gag”) reflex is evaluated by stimulating the
posterior pharyngeal wall on each side with a sterile, blunt object
(e.g. by cotton wool bud), but the reflex is sometimes absent in
normal individuals.
• IX, X: Palate (uvula) in rest in the midline position,
• lifts symetrically during phonation,
• no dysarthria, no dysphonia (hoarse voice)
• Palate reflex: particular (left or right) palatine arch lifts slighly in a
response to slight touch of particular arch
http://clinicalexams.co.uk/
EXAMINATION OF CRANIAL
NERVES – XI – accesory nerve
• The spinal accessory nerve innervates the
sternocleidomastoid and trapezius muscles.
• The sternocleidomastoid is tested by asking
the patient to rotate the head against
resistance provided by the examiner’s hand,
which is placed on the patient’s jaw.
Sternocleidomastoid weakness results in
decreased ability to rotate the head away
from the weak side.
• The trapezius is tested by having the patient
shrug the shoulders against resistance and
noting any asymmetry.
http://en.wikipedia.org/
EXAMINATION OF CRANIAL
NERVES – XII - hypoglossal
• The hypoglossal nerve innervates the tongue muscles.
• It can be tested by having the patient push the tongue against
the inside of the cheek while the examiner presses on the
outside of the cheek. With unilateral tongue weakness, the
ability to press against the opposite cheek is reduced.
• There may be also deviation of the protruded tongue toward
the weak side, although facial weakness may result in falsepositive
tests. Tongue weakness also produces dysarthria with
prominent slurring of labial sounds.
• Finally, denervation of the tongue may be associated with
wasting (atrophy) and twitching (fasciculation).
http://wikivisually.com/
Cranial nerves
• I. Olfactory nerve
• II. Optic nerve
• III. Oculomotor nerve
• IV. Trochlear nerve
• V. Trigeminal nerve
• VI. Abducens nerve
• VII. Facial nerve
• VIII. Vestibulocochlear nerve
• IX. Glossopharyngeal nerve
• X. Vagus nerve
• XI. Accessory nerve
• XII. Hypoglossal nerve
Teachmeanatomy.info
Intracranial
hypertension
Intracranial pressure
• Intracranial pressure is the pressure exerted by fluids such as
cerebrospinal fluid inside the skull and on the brain tissue.
Normal pressure is 7–15 mmHg for a supine adult.
• The body has various mechanisms by which it keeps the ICP
stable, with CSF pressures varying by about 1 mmHg in normal
adults through shifts in production and absorption of CSF.
Changes in ICP are attributed to volume changes in one or more
of the constituents contained in the cranium.
Intracranial
hypertension
• Intracranial hypertension is elevation of the
pressure in the cranium. ICP is normally 7–15
mm Hg; at 20–25 mm Hg, the upper limit of
normal, treatment to reduce ICP may be needed.
• Headache, worse in laying-down position.
• Vomiting – sudden without nausea
• Vertigo
• Papiledema
• Bradykardia
• VI. Nerve palsy
• Epileptic seizures
• Consciousness disturbances
http://sei80.com/
Brain herniation
• Brain herniation is a potentially deadly side
effect of very high pressure within the skull that
occurs when a part of the brain is squeezed
across structures within the skull.
• The brain can shift across such structures as the
falx cerebri, the tentorium cerebelli, and even
through the foramen magnum.
• Herniation can be caused by a number of factors
that cause a mass effect and increase intracranial
pressure:
• traumatic brain injury
• intracranial hemorrhage
• brain tumor
• etc.
http://emergencymedicinecases.com/
Brain herniation
• Brain herniation is classified based on the structure through which tissue is
herniated:
• Transtentorial (uncal) herniation: The medial temporal lobe is squeezed
by a unilateral mass across and under the tentorium that supports the
temporal lobe. N III. Palsy and homolateral mydriasis.
• Subfalcine herniation: The cingulate gyrus is pushed under the falx cerebri
by an expanding mass high in a cerebral hemisphere resulting to
compression of a. cerebri anterior.
• Central herniation: Both temporal lobes herniate through the tentorial
notch because of bilateral mass effects or diffuse brain edema.
• Upward transtentorial herniation: This type can occur when an
infratentorial mass compresses the brain stem, kinking it and causingbrain
stem ischemia.
• Tonsillar herniation: Usually, the cause is an expanding infratentorial mass
(eg, cerebellar hemorrhage), forcing the cerebellar tonsils, through the
foramen magnum and death.
http://radiopaedia.org/
Intracranial hypotension
• Intracranial hypotension is a condition in which there is negative pressure within the
brain cavity.
• There are several possible causes:
• Cerebrospinal fluid (CSF) leak from the spinal canal: A leak following a lumbar
puncture.
• A defect in the dura mater.
• A congenital weakness.
• Following spinal surgery.
• Following spinal trauma.
• Ventriculoperitoneal shunt with a low pressure valve.
• In some cases, spinal CSF leaks can lead to a descent of the cerebellar tonsils
into the spinal canal, similar to a Chiari malformation.
• The classic symptom is severe headache when upright, which is relieved when lying
flat. Other symptoms can include nausea, vomiting, double vision and difficulty with
concentration.
Consciousness
disturbances
Consciousness
disturbances
• Consciousness is awareness of the internal and external
world, and the level of consciousness is described in terms of
the patient’s apparent state of wakefulness and response to
stimuli.
• A patient with a normal level of consciousness is awake (or
can be easily awakened), alert (responds appropriately to
visual or verbal cues), and oriented (knows who and where he
or she is and the approximate date and time).
• Abnormal consciousness represents a continuum ranging
from mild sleepiness to unarousable unresponsiveness
(coma).
• Depressed consciousness should be characterized more
precisely in terms of the stimulus–response patterns
observed.
• Progressively more severe impairment of consciousness
requires stimuli of increasing intensity to elicit increasingly
primitive (nonpurposeful or reflexive) responses
• Assessed while recording the history.
http://wikivisually.com/
Consciousness disturbances
TWO TYPES OF ALTERATION OF THE CONSCIOUSNESS (a state of awareness of self and
surroundings):
• The first type AFFECTS AROUSAL (sometimes called „quantiatative“)
• described on four levels (not very accurate –continuum of subtly changing status)
• ALERT – perfectly normal state of arousal
• LETHARGY (drowsinness) – between alertness and stupor („sleepy“, fine stimuli enough)
• STUPOR – a state of baseline unresponsiveness that requires repeated application of vigorous
stimuli to achieve arousal
• COMA - coma is a state of complete unresponsiveness to arousal, in which the patient lies
with the eyes closed
THE GLASGOW COMA
SCALE
• Widely used scale to assess the initial
severity of traumatic brain injury.
• Separate assessment of three aspects of a
patient's behavior:
• the stimulus required to induce eye
opening
• the best motor response
• the best verbal response
• Each symptom is scored, sum score is
obtained.
• Simple and reproducible.
• An ideal method of assessment for nonneurologists
involved in the care of comatose
patients.
• Limited use in patients who are intubated or
who have suffered facial trauma or have
aphasia.
Consciousness
disturbances
• The second type INVOLVES
COGNITIVE AND AFFECTIVE
MENTAL FUNCTION
• sometimes referred to as the
“content” of mental function
• dementia, delusions, confusion
http://dementiaguide.ca/
Delirium
• Delirium, also known as “acute confusional state“, is
an organically caused decline from a previous baseline
mental functioning that develops over a short period
of time, typically hours to days.
• Delirium is a syndrome encompassing disturbances in
attention, consciousness, and cognition. It may also
involve other neurological deficits, such as
psychomotor disturbances (e.g. hyperactive,
hypoactive, or mixed), impaired sleep-wake cycle,
emotional disturbances, and perceptual disturbances
(e.g. hallucinations and delusions), although these
features are not required for diagnosis.
• Delirium is caused by an acute organic process, which
is a physically identifiable structural, functional, or
chemical problem in the brain that may arise from a
disease process outside the brain that nonetheless
affects the brain.
• Delirium x delirium tremes!
symptoma.com
EXAMINATION
OF THE
COMATOSE
PATIENT
The examiner should first assess the degree of coma (The Glasgow
Coma Scale).
If the patient is determined to be in coma based on the GCS <8, the
examiner should then determine whether brain stem functions are
intact.
Breathing - From cranial to caudal:
•Cheyne-Stokes respiration – a pattern of alternating hyperventilation and
hypoventilation seen with bilateral cerebral dysfunction or basal ganglia lesions.
•Central neurogenic hyperventilation, produces rapid respiratory rate of up to 40-
70/minute and is seen with midbrain dysfunction.
•Apneustic breathing refers to slow breathing with a prolonged pause after
inspiration. This occurs with pontine dysfunction.
•Ataxic (Biot’s ) respirations refer to irregular respiratory frequency and amplitude
and indicates medullary dysfunction with impending respiratory arrest.
•The respiratory patterns may occur in a step-wise pattern in transtentorial
herniation.
EXAMINATION OF THE
COMATOSE PATIENT
• Pupillary Reactions: Examination should be aimed at determining the size of
each pupil and its direct and consensual reaction to the light. The size and
equality of the pupils may give localizing clues.
• Eye Movements:
• Sustained lateral conjugate deviation of the eyes suggests disease of the
ipsilateral cerebral hemisphere or contralateral pons.
• Downward deviation of the eyes with convergence is seen with thalamic
or dorsal midbrain lesions.
• Ocular bobbing (rapid downward movements, slow return to primary
position) classically occurs with pontine lesions.
•
Corneal Reflex: The corneal reflex tests the reflex arc of V1 to VII.
• The afferent limb tested via corneal stimulation via the opthalamic
division of the trigeminal nerve (V1).
• The efferent limb in the contraction of the obicularis oculi (VII).
http://kaltura.com/
EXAMINATION
OF THE
COMATOSE
PATIENT
Ganong's Review of Medical Physiology - Kim E. Barrett et al., 25th Edition.
Diagnosis of brain death
– neurology examination
• Components of a complete neurological examination are:
• Examination of the patient-absence of spontaneous
movement, decerebrate or decorticate posturing,
response to verbal stimuli, and response to noxious
stimuli administered through a cranial nerve pathway.
• During the examination spinal reflexes may be present.
• Absent pupillary reflex.
• Absent corneal, oculocephalic, cough and gag reflexes.
• Absent oculovestibular reflex when tested with 20 to 50
ml. Of ice water irrigated into an external auditory canal
clear of cerumen, and after elevating the patients head
30'. Labyrinthine injury or disease, anticholinergics,
anticonvulsants, tricyclic antidepressants, and some
sedatives may alter response.
http://wikilectures.eu/
Vertebral
column
examination
http://anatomychartee.co/
A typical Vertebra – anatomy
(superior view)
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
Vertebral column
examination
• The normal spine has a cervical and lumbar lordosis, and a
thoracic kyphosis. Exaggeration of these normal
alignments may result in hyperkyphosis of the thoracic
spine or hyperlordosis of the lumbar spine.
• Inspection may reveal a lateral curvature of the spine
(scoliosis) or an asymmetry in the prominence of the
paraspinal muscles, suggesting muscle spasm.
• Back pain of bony spine origin is often reproduced by
palpation or percussion over the spinous process of the
affected vertebrae.
• The neurologic examination includes a search for focal
weakness or muscle atrophy, or signs of spine injury.
https://encyclopedia.nm.org/
Vertebral column
examination
• Lasegue sign
• Among the most helpful signs in detecting nerve root
compression is passive straight-leg raising (possible up
to almost 90 degrees in normal individuals) with the
patient supine.
• This maneuver is the usual way in which compression of
the LS or Sl nerve root is detected.
• Thomayer test
• Schober's test
• While the patient is in a standing position the examiner
makes a mark approximately at the level of L5. Two
points are marked: 5 cm below and 10 cm above this
point (for a total of 15 cm distance). Then the patient is
asked to touch his toes while keeping the knees
straight. If the distance of the two points do not
increase by at least 5 cm (with the total distance
greater than 20 cm), then this is a sign of restriction in
the lumbar flexion.
Cs.wikipedia.org; http://nle.nottingham.ac.uk/; George V. Lawry, Adel G. Fam, et al. Fam's Musculoskeletal Examination and Joint Injection Techniques (Second Edition), 2010.
Terminology of
spinal
degenerative
changes
SPONDYLOSIS (IN THE
BROAD SENSE) –a
complex of degenerative
and proliferative changes
of the spinal column
SPONDYLOSIS (IN THE
STRICT SENSE) –
proliferative changes in
spinal vertebrae bodies
with formation of
osteophytes
SPONDYLATRHROSIS
(SPONDYLARTHROPATHY)
– degenerative changes of
intervertebral joints (so
called facet joints)
INTERVERTEBRAL DISC
DISORDERS deterioration,
herniation
or other dysfunction of
intervetrebral disc
(secondary degenerative
disc disease)
Patophysiology of
degenerative changes
• MULTIFACTORIAL
• Usually starts in intervertebral DISC
• Following FACTORS may influence spinal degeneration
development and progression :
• age
• smoking
• mechanical overload
• traumatic spinal injuries
• genetical factors
• Clinical manifestation of spondylosis is mainly dependent of
CONGENITAL SPINAL CORD WIDTH.
Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
Clinical
manifestation
of
spondylogenic
disorders
So called SEGMENTAL SYNDROME (spine
blockage) (e.g. lumbago)
• Pain + spinal dysfunction (block or hypermobility)
• = functional spondylogenic disorders
NON-RADICULAR SYNDROMES WITH IRADIATION
OF PAIN ALONG THE RADICULAR ZONES
• Pain iradiading from spine to extremities or thorax, not
specificaly in radicular distribution
• No objetive symptoms of radicular lesion
COMPRESIVE SPONDYLOGENIC SYNDROMES
• radiculopathy (radicular dysfunction)
• Or myelopathy (spinal cord dysfunction)
• About 1/10 of all back pains
Clinical
presentation of
radiculopathies
SENSORY SYMPTOMS
• Positive:
• Pain „radiated“ along the dermatome
(evaluate by NRS)
• Other: paresthesia, dysesthesia
• Negative
• Hypesthesia
MOTOR SYMPTOMS
• Paresis in particular myotome
• hypo-areflexia of particular deep tendon
reflexes
• Muscle hypotrophy
Cervical spine Clinical
syndromes
SEGMENTAL SYNDROME – cervical spine blockage
NON-RADICULAR IRADIATING PAIN
• CERVICOBRACHIAL SYNDROME
• Very frequent, emotional accompaniment
• The most frequent cause = intervertebral joint affection
COMPRESIVE SPONDYLOGENIC SYNDROMES
• CERVICAL RADICULOPATHY (see below)
• SPONDYLOGENNIC CERVICAL MYELOPATHY
• Cervical spinal cord dysfunction
• Usually quadriparesis (quadriplegia)
• Most frequently upper motor neuron affection in LE
• + upper and/or lower motor neuron affection in UE
• Spastic gait, clumsy hand
• Cervical spinal pain – may not be present
http://mauritius-images.com/
Thoracic spine:
Clinical
syndromes
• Quite frequent
SEGMENTAL SYNDROME – thoracic spine block
• Usually caused by intervertebral joint blockage in thoracic
spine region WITH NON-RADICULAR IRADIATION
• RARELY RADICULOPATHY (mostly secondary – radiculiris,
postherpetic neuralgia).
INTERCOSTAL NEURALGIA
• Very rare
• Presenting by spastic paraparesis:
• upper motor neuron signs (weakness, spasticity, cltered
tonus)
• pathological hyperreflexia and Babinsky sign
• sensory loss – sensory level (Nipples T4, umbilicus T10)
• bowel/bladder symptoms and sexual dysfunction
SPONDYLOGENNIC THORACIC MYELOPATHY
Lumbar spine: Clinical
syndromes
• Very frequent !!!
• SEGMENTAL SYNDROME: LOW BACK PAIN – very frequent
• NON-RADICULAR IRADIATING PAIN
• Low back pain
• Pain radiates into the buttocks and legs
• No objetive symptoms of radicular lesion
• RADICULAR SYNDROMES
• SCIATICA: any pain starting in the lower back and going down the leg
• In Czech literature (not used in English)
• LUMBOISCHIALGIC SYNDROME – L5 or S1 radiculopathy
• Most frequent
• LUMBOFEMORAL SYNDROME -L3 or L4.radiculopathy
Bell S.E., Beauchamp K.M. (2012) Conus Medullaris Syndrome. In: Vincent JL., Hall J.B. (eds) Encyclopedia of Intensive Care
Medicine. Springer, Berlin, Heidelberg
Resources
• Harrison's Neurology in Clinical Medicine - 3th Edition. Stephen
Hauser, S. Andrew Josephson.
• Lange Clinical Neurology - 10th Edition. Roger P. Simon, David
Greenberg, Michael J. Aminoff.
• Adams and Victor's Principles of Neurology - 10th Edition. Allan
Ropper, Martin Samuels, Joshua Klein.
• Netter's Clinical Anatomy - 4th Edition. John T. Hansen.
Thank you for your attention
Kolcava.Jan@fnbrno.cz