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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3230_Библиотеки_им_академика_М_И_Перельмана
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CHAPTER 13 Neurological signs
322
Large (mydriatic) pupil with no ptosis
Some differential diagnoses and typical outline evidence
Holmes–Adie
pupil
due to ciliary
ganglion
degeneration
Suggested by: dilated pupil (often widely) that only
reacts slowly to light by constricting in well-lit room
after 30 minutes. Reacts to accommodation. Usually
unilateral. Absent knee jerks. Usually in females
Confirmed by: benign outcome with no action
necessary
Traumatic
iridoplegia
Suggested by: history of direct trauma. Dilated, fixed,
irregular pupil that does not accommodate or react to
light
Confirmed by: slit-lamp examination of anterior eye
chamber
Drug effect
due to cocaine,
amphetamines,
tropicamide,
atropine
Suggested by: bilateral pupil dilation
Confirmed by: drug history, and resolution with
withdrawal
Severe
brainstem
dysfunction
(or brain death)
Suggested by: bilateral pupil dilation with no reac
t
ion to
light, comatose, long tract pyramidal signs
Confirmed by: absent corneal reflex response, no vesti-
bulo-ocular reflexes, no cranial motor response to
stimulation, no gag reflex, insufficient respiratory effort
when PCO
2
>50 mm Hg to prevent further i of PCO
2
and dPO
2
SMALL (MIOTIC) PUPIL WITH NO PTOSIS1
323
Small (miotic) pupil with no ptosis
Some differential diagnoses and typical outline evidence
Argyll Robertson
pupil
(due to syphilis
and diabetes
mellitus, rarely)
Suggested by: unilateral, small, irregular pupil that
accommodates by constricting when focusing on near
finger but does not react to light
Confirmed by: syphilis serology or fasting blood glucose
≥7 mmol/L and random GTT glucose ≥11.0 mmol/L.
Positive syphilis serology or abnormal blood glucose
suggesting diabetes mellitus
Anisocoria
normal variation
Suggested by: unilateral, small, miotic pupil that reacts
normally to light and accommodation
Confirmed by: no change with time, benign outcome
with no action necessary
Age-related
miosis
due to
autonomic
degeneration
Suggested by: bilateral, small, miotic pupils that react
normally to light and accommodate normally
Confirmed by: discovery in old age, no change with
time, benign outcome with no action
Drug effect
due to opiates,
pilocarpine
Suggested by: bilateral, small pupils. Not reacting
to light
Confirmed by: drug history, and resolution with
withdrawal
Pontine
hemorrhage
Suggested by: bila
t
eral, small, miotic pupils that react to
light. Patient comatose, bilaterally or unilaterally
hyperreflexic, with high or fluctuating temperature.
Confirmed by: evolution of signs to localize to brain
stem. MRI scan
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CHAPTER 13 Neurological signs
324
Squint and diplopia: ocular palsy
This is elicited by asking the patient to follow the examiner’s finger and
asking if this results in seeing double, and looking for development of a
convergent or divergent squint.
For a cover test, have the patient fix focus in the distance and alter-
nately cover either eye in quick succession. As the cover is lifted observe
the eye. If the uncovered eye now moves in, this indicates a divergent
squint. If the eye moves out, this indicates a convergent squint.
Some differential diagnoses and typical outline evidence
Oculomotor
(third-nerve)
paresis
intracavernous or
posterior com-
municating artery
aneurysm, men-
ingioma, tentorial
pressure cone,
DM, syphilis, and
brain stem
ischemia
Suggested by: ptosis, diplopia and squint maximal on
looking up and in; but therefore in total loss eye
looks down and out. Dilated pupil (except in diabetes
mellitus, syphilis and brain stem ischemia when pupil
not dilated)
Confirmed by: other cranial nerve lesions that form a
pattern (see p. 332), skull X-ray posterior–anterior
(P-A) and lateral, CT or MRI scan appearance
Trochlear
(fourth cranial
nerve) paresis
Suggested by: diplopia and squint maximal on looking
down and in. Double vision for reading and walking
down stairs
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
Abducent (sixth
cranial nerve)
paresis
Suggested by: double vision when looking in direction
of the affected muscle. Head turn in direction of
affected muscle
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
Myasthenia
gravis, Graves’
disease, orbital
cellulitis, or
tumor
Suggested by: diplopia and squint in all directions
of gaze
Confirmed by: CT or MRI scan of orbit or positive
Tensilon test (edrophonium results in less diplopia
and squint in myasthenia)
Internuclear
ophthalmoplegia
from lesion in
medial longitudi-
nal bundle,
usually due to
MS or sometimes
vascular
Suggested by: impaired conjugate gaze (slowness of
adducting eye and nystagmus in abducting eye)
Confirmed by: other signs of brain stem lesion
LOSS OF FACIAL SENSATION1
325
Loss of facial sensation
Some differential diagnoses and typical outline evidence
Ophthalmic
branch of
trigeminal
nerve lesion
Suggested by: absent corneal reflex (present corneal
reflex excludes lesion) with diminished touch and pain
sensation in upper face above the line of the eye
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
Maxillary branch
of trigeminal
nerve lesion
Suggested by: diminished touch and pain sensation in
mid-face between line of mouth and line of eye
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
Mandibular
branch of
trigeminal
nerve lesion
Suggested by: diminished touch and pain sensation in
lower face below line of mouth
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
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CHAPTER 13 Neurological signs
326
Jaw muscle weakness
Some differential diagnoses and typical outline evidence
Motor branch
of trigeminal
nerve (fifth
cranial): lower
motor neuron
type on same
(ipsilateral) side
Suggested by: weakness of jaw movement. Devia
t
ion of
jaw when opening against resistance and poor contrac-
tion of masseter on clenching. Decreased jaw jerk
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
Motor branch
of trigeminal
nerve (fifth
cranial): upper
motor neuron
type on other
(contralateral)
side
Suggested by: weakness of jaw movement. Deviation
of jaw when opening against resistance and poor
contraction of masseter on clenching. Increased
jaw jerk
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332). MRI scan appearance
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Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
CHAPTER 13 Neurological signs
328
Facial muscle weakness
Distinguish between upper (forehead muscles movement preserved) and
lower (forehead movement weak) motor neuron type.
Some differential diagnoses and typical outline evidence
Facial nerve
palsy (seventh
cranial): upper
motor neuron
type, other
(contralateral)
side
due to internal
capsule lesion—
cerebrovascular
accident, tumor
Suggested by: able to raise eyebrows and close eye,
but unable to grimace or smile symmetrically; other
cranial nerve lesions that form pattern (see p. 332)
Confirmed by: MRI scan
Facial nerve
palsy (seventh
cranial): lower
motor neuron
type, same
(ipsilateral) side
(see below for
causes)
Suggested by: inability to raise eyebrows nor close eye
(rolls upwards to hide iris revealing the white of the
eye) nor grimace nor smile symmetrically; other
cranial nerve lesions that form pattern (see p. 332)
Confirmed by: MRI scan
Bell’s palsy Suggested by: lower motor neuron seventh-nerve
palsy. Prior ache behind ear. No other physical signs
(corneal reflex present and no deafness or vertigo)
Confirmed by: above clinical features
Ramsey Hunt
syndrome
Suggested by: lower motor neuron seventh-nerve
palsy. Taste diminished on same side. Vesicles in
external auditory meatus
Confirmed by: above clinical features
Facial nerve
palsy from
parotid swelling
Suggested by: lower motor neuron seventh-nerve
palsy. Swelling in mid-face on same side
Confirmed by: above clinical features and MRI scan
FACIAL MUSCLE WEAKNESS1
329
Cerebellopontine
lesion (e.g., tumor)
Suggested by: lower motor neuron seventh-nerve
palsy. Associated fifth (loss of corneal reflex) and
seventh cranial nerve lesion
Confirmed by: above clinical features. MRI scan
appearance
Cholesteatoma Suggested by: lower motor neuron seventh-nerve
palsy. Also deafness and vertigo
Confirmed by: above clinical features. MRI scan
appearance
Facial nerve palsy
from
demyelination
Suggested by: lower motor neuron seventh-nerve
palsy. Other focal neurological signs and symptoms
disseminated in time and space
Confirmed by: above clinical features. MRI scan
appearance
Facial nerve palsy
from brain stem
ischemia
Suggested by: lower motor neuron seventh-nerve
palsy. Signs of adjacent dysfunction, e.g., nystagmus,
long tract signs, e.g., spastic hemiparesis
Confirmed by: above clinical features. MRI scan
appearance
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CHAPTER 13 Neurological signs
330
Loss of hearing
The patient is unable to hear whispering or a ticking watch. Test hearing
with a tuning fork held near the ear; test both air and bone conduction.
Some differential diagnoses and typical outline evidence
Eighth-nerve
conduction
defect on side X
due to wax,
foreign body,
otitis externa,
recurrent otitis
media, injury
to tympanic
membrane,
otosclerosis,
cholesteatoma
Suggested by: forehead vibration heard louder on side
X than on side Y (Weber
’s test), and mastoid vibra
t
ion
on side X louder than for air (Rinne
’s test)
Confirmed by: auroscope appearance, formal audiometry,
and other cranial nerve lesions that form pattern
(see p. 332). MRI scan appearance
Sensorineural
(eighth cranial)
lesion on side Y
due to old age,
noise trauma,
Paget’s disease,
Menier’s disease,
drugs, viral
infections (e.g.,
measles), con-
genital rubella,
meningitis,
acoustic
neuroma,
meningioma
Suggested by: forehead vibration heard louder on side
X than on side Y (Weber
’s test), and mastoid vibra
t
ion
same for both sides (Rinne
’s test)
Confirmed by: other cranial nerve lesions that form
pattern (see p. 332), formal audiometry, and MRI scan
appearance
ABNORMAL TONGUE, UVULA, AND PHARYNGEAL MOVEMENT1
331
Abnormal tongue, uvula, and
pharyngeal movement
This implies ninth, tenth (not eleventh), and twelfth cranial nerve lesions.
Some differential diagnoses and typical outline evidence
Glossopharyngeal
(ninth
cranial)
nerve lesion
Suggested by: loss of gag reflex and taste on posterior
1/3 of tongue; other cranial nerve lesions that form
pattern (see p. 332)
Confirmed by: MRI scan
Vagus (tenth
cranial) nerve
lesion
due to jugular
foramen lesion,
bulbar palsy
Suggested by: deviation of uvula away from affected
side when saying
“ah”; nasal regurgitation of water.
Dysarthria; other cranial nerve lesions that form
pattern (see p. 332)
Confirmed by: MRI scan
Lower motor
neuron
hypoglossal
(twelfth
cranial)
nerve lesion
on same
(ipsilateral) side
of deviation
Suggested by: deviation of tongue to side of lesion on
protrusion. Fasciculation and wasting; other cranial
nerve lesions that form pattern (see p. 332)
Confirmed by: MRI scan
Upper motor
neuron
hypoglossal
(twelfth
cranial)
nerve lesion
on other
(contralateral)
side of deviation
Suggested by: deviation of tongue to one side on
protrusion. Small, stiff tongue and cortical or
internal capsule signs
Confirmed by: CT or MRI scan
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