Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2548_Библиотеки_им_академика_М_И_Перельмана
.pdf
318
https://t.me/med1917
15
Locomotor system
Figure 15.63 Computed tomography (CT) scan of sacroiliac
joints, showing a distinctive lesion on the left side with a
sequestrum owing to tuberculosis.
Figure 15.62 (A) Synovial thickening seen as hypoechoic (darker
grey) material over the dorsal aspect of the metacarpal head and
neck using ultrasound. (B) Power Doppler signal seen as red/
orange signal located within the synovial thickening within the
metacarpal- phalangeal joint.
characterized on CT imaging (e.g. malignancy,
erosive disease or fracture). MRI has unique
advantages in evaluating the musculoskeletal
system, but it is vital that the clinician defines
the pathology suspected, as correct positioning
and sequence selection (T- weighting) are vital in
optimizing image quality. MRI is increasingly used
to image the major joints in the limbs, especially
the knee (see Fig. 15.47), hip, shoulder and elbow.
In the context of inflammatory arthritis, MRI has
much to recommend it as an imaging modality. There
is a clear relationship with bone marrow oedema on
MRI and the subsequent development of erosive
arthritis providing an early indicator of potentially
poor prognosis. Erosive disease, when present,
is detected earlier than with plain radiographs
and changes in synovial inflammation can be
readily detected after therapeutic intervention. A
standardized, validated scoring system has been
developed (RAMRIS: Rheumatoid Arthritis MRI
Scoring), which encompasses multiple elements
of MRI-detected synovial inflammation and joint
damage.
Figure 15.64 A lumbar spine magnetic resonance imaging (MRI)
scan. There is a disc protrusion at L4/5 with degeneration of the
disc itself, shown by the less bright signal in the intervertebral disc
at this level.
use of intravenousEnhancement by the
paramagnetic contrast (e.g. gadolinium) has further
improved definition in spinal imaging.
invaluableisimagingresonanceMagnetic
when assessing the degree of spinal involvement
in spondyloarthropathies, such as ankylosing
spondylitis, particularly in early disease where
radiography ankylosis is absent. Both costovertebral
SECTION THREE
WWW.BOOKBAZ.IR
https://t.me/med1917
Locomotor system
319
Figure 15.65 Magnetic resonance image (MRI) of cervical spine in a patient with transverse myelitis owing to systemic lupus
erythematosus (SLE) (A) before and (B) after immunosuppression.
and sacroiliac joints are readily imaged with good
sensitivity for inflammatory pathology.
It is of particular value in the non- invasive
investigation of disc disease (Fig. 15.64), including
spinal infection, and is a sensitive technique for
the diagnosis of avascular necrosis. MRI scanning
of the brain and spine is the single most important
investigation in neuroimaging, as the neural tissues
themselves, together with supporting tissues, are
well visualized. Bone is less well seen with this
technique. As a rule of thumb, most abnormalities
appear dark on T1- weighted images and white on
T2- weighted images. Some common problems are
shown in Figures 15.55, 15.64 and 15.65.
Isotopic scanning (scintigraphy) can be used in the
diagnosis of acute (e.g. infection or stress fracture)
or multiple (e.g. metastases) bone lesions by use
of the first 2- minute (dynamic blood flow) phase,
second 10- minute (blood pool) phase and third
3- hour late phase (osteoblastic) (Fig. 15.66)
following intravenous injection of diphosphonate
compounds. Tomographic scintigraphy can
further refine definition of the isotope uptake
(e.g. in stress fracture of the pars interarticularis).
Radionucleotide bone scans are more sensitive
than plain radiographs for the diagnosis of Paget’s
disease and in polyostotic cases help to quantify
the overall burden of disease. Scintigraphy has a
high sensitivity to metabolically active lesions;
however, it is relatively non- specific and is often
used in conjunction with other imaging modalities.
Dual- energy X- ray absorptiometry (DEXA) is
widely
used to assess bone mineral density in
metabolic bone disease and osteoporosis. Scans
recorded with long intervals (e.g. every 2 to 3
years) between them may be used to assess the
320
https://t.me/med1917
15
Locomotor system
Figure 15.66 Technetium bone scan in a distance runner,
showing focally increased uptake in the lower tibia owing to a
stress fracture.
effects of therapy. Results are expressed in relation
to a normal reference range.
Positron emission tomography (PET) scanning
is becoming more widely available, but remains
expensive. This is a type of scintigraphic
molecular imaging based mostly on the uptake
of radiolabelled glucose by metabolically
active structures. PET scans are mostly used in
rheumatology investigations and have better
signal- to- noise ratio than standard isotope
bone scanning. The combined technology of
CT and PET scanning allows the acquisition
of structural information simultaneously with
metabolic activity. It is extremely sensitive in
detecting malignancy and is also proving useful
in documenting large vessel inflammation in
disorders such as Takayasu’s arteritis and giant cell
arteritis. The radiation exposure is considerable
and, as such, this imaging modality should be used
cautiously and appropriately.
SECTION THREE
WWW.BOOKBAZ.IR
https://t.me/med1917
BASIC SYSTEMS
Nervous system
Rodney W.H. Walker and David A. Gallagher
16
Introduction
In recent years impressive advances have been made
throughout the field of neurology—in delineating
disease entities and understanding their aetiology
and pathogenesis; in diagnostic methods, particularly
imaging and genetic testing; and in treatment and
management. However, despite advances in investigations, careful clinical assessment remains of central
importance.
The fundamental importance of the clinical history and examination cannot be overemphasized.
In the diagnosis of neurological disease, it is the
history, rather than the examination, that is paramount, so it is even more important for this to be
comprehensive. History taking has not changed
significantly, but clinical neurological examination continues to evolve. Significant contributions
have come from clinical assessment scales, some of
which have been so successful as to have become
internationally institutionalized, for example the
Glasgow Coma Scale and the Mini- Mental State
Examination (although the latter has recently been
patented). On the other hand, clinical signs of limited sensitivity, specificity, reliability and localizing
value can be dispensed with.
A thorough neurological examination does involve
doing more than is the case for other systems. Some
basic neuroanatomical knowledge is necessary, but
most clinical neurology need not be daunting. In
new patients presenting for diagnosis, a sensible
formulation of the nature of the problem on the
basis of the history and examination is critical in
order to request appropriate investigations, should
they be necessary. Modern imaging undoubtedly
has been the biggest revolution in clinical neurology
in recent years, but injudicious use of imaging
frequently leads to confusion, delay in diagnosis and
sometimes harm. Similar considerations apply to the
other major investigational modalities.
This chapter will discuss some aspects of neurological
history, concentrate on neurological examination and
the formulation of the nature of the neurological
diagnosis and include some remarks on neurological
investigations. Coma, delirium and dementia are not
covered in this chapter.
The neurological history
The essentials of history taking have been covered
elsewhere, but some points are particularly salient to
neurological conditions. The repertoire of neurological symptoms is actually quite limited, although perhaps larger than that of other specialties. Box 16.1
lists the usual ones that you should specifically ask
about in taking a neurological history.
The time course of evolution and sometimes resolution of neurological symptoms very frequently indicate the nature of the problem, and so they need to
be clarified as precisely as possible. Thus, sensory or
motor symptoms, which start abruptly and are at their
most marked at or very soon after their onset, strongly
suggest a vascular causation (transient ischaemia or
ischaemic or haemorrhagic stroke). In contrast, similar
symptoms evolving over a few days, reaching a plateau
in severity and then slowly receding typify inflammatory central nervous system (CNS) demyelination (a
first episode or a relapse of multiple sclerosis). Subacute (developing over weeks to months), progressive
symptoms can be caused by many kinds of pathology,
but neoplasia is always a prime concern.
These statements are true enough to be clinically
useful, although there are exceptions. For example,
one of the reasons for requesting cranial imaging in
all cases of stroke is to exclude a benign or malignant tumour or other pathology, which has caused
a stroke- like presentation. Neurodegenerative conditions always develop insidiously with gradual progression, but occasionally patients present acutely.
For example, motor neuron disease can present
acutely with ventilatory failure. Alzheimer’s disease
commonly becomes evident after an episode of acute
delirium caused by an intercurrent illness. Sometimes, gradually progressive neurological conditions
seem to present suddenly, and only when they begin
to interfere with the patient’s daily functioning.
Two common neurological presentations require a
history, not only from the patient but also, if at all
possible, from others: attacks of loss of consciousness
and memory impairment.
The three most common causes of attacks of reduced
consciousness or awareness that lead to neurological
consultations are neurocardiogenic syncope, epilepsy
322
https://t.me/med1917
16
Nervous system
Box 16.1
Cognitive symptoms, especially memory impairment
Headache
Loss of awareness
Loss of consciousness
Alteration of perception, including déjà vu
Dizziness, vertigo
Loss of balance
Falls
Loss of sense of smell
Loss of taste
Loss of vision
‘Positive’ visual symptoms, including components of
Double vision
More than double vision (polyopia, palinopsia)
Oscillopsia (a visual sensation of stationary objects
Deafness
Tinnitus
Difficulty with speech
Difficulty swallowing
Weakness
Abnormal movements of muscles (including cramp,
Abnormal movements of parts of the body (including
Clumsiness
Impairment of control of limbs
Altered sensation
Loss of sensation
Pain
Symptoms of postural hypotension
Impairment of sexual function
Impairment of bladder control
Impairment of bowel control
Neurological symptoms
migraine auras, unformed and formed hallucinations
swaying back and forth)
fasciculations)
tremor, dystonia, myoclonus)
and psychogenic non- epileptic attacks. It is far more
informative to hear a description from a witness than
to request potentially misleading and inappropriate
investigations. Obtaining the witness’s account may
require a telephone call; this is time well invested.
Table 16.1 summarizes some points, which help
to distinguish syncope from seizures. In the case of
recurrent attacks, asking patient’s friends or relatives
to record the episode, for example on a mobile phone
camera, can be invaluable, particularly in psychogenic
non- epileptic attacks.
Memory impairment is a common complaint. Distinguishing between the worried, but well, and those
with real impairment is greatly facilitated by information provided by close family or other informants.
In general, if a patient is brought to a doctor by a
relative who complains that the patient has memory
impairment, there is most often an organic disorder, usually dementia. In contrast, many but not all
patients who come to a doctor alone with the same
complaint have good cognitive function. Furthermore, it is the relative who can report on changes in
personality, behaviour, self- care and capacity, which
may be crucial to the diagnosis.
The most frequent symptom leading to neurological referral is headache. It is also a common reason for
attending an emergency department. The vast majority
of headaches are not caused by life- threatening disorders, such as aneurysmal subarachnoid haemorrhage,
meningitis or brain tumour, but are caused by common
primary headache syndromes, particularly migraine.
Table 16.2 outlines some of the features, which may
help to distinguish headaches of different sorts.
Vertigo (a hallucination of movement) is an important symptom that requires careful characterization. It
indicates a disorder of one or both labyrinths, vestibular
nerves, vestibular nuclei in the brainstem or, rarely, the
Table 16.1 Points that help to distinguish syncope from seizures involving loss of consciousness. Minor injury, incontinence and
sleepiness after the event do not distinguish well.
Syncope Seizure
In neurocardiogenic syncope, characteristic prodromal
features include: tinnitus, muffled hearing, dimming of
vision, loss of vision while still conscious, widespread
altered sensation, dizziness (may be described as spinning),
lightheadedness, feeling of impending faint, weakness
Marked pallor
Sweating (but not in those with autonomic failure)
Any convulsion is brief (seconds)
Rapid recovery of lucidity and memory (registration and
recall)
Patient comes round on the ground where he fell
A second attack immediately on being sat up after the first
attack is very suggestive of neurocardiogenic syncope
Neurocardiogenic syncope is commonly set off by pain,
squeamishness, gastrointestinal illness, public places
indoors (clubs, restaurants, trains), prolonged standing
The symptoms of focal seizure activity which precede a secondarily
generalized attack may or may not be remembered after the attack is
over. For example, sensory hallucinations (olfactory, gustatory, visual,
auditory or somatosensory) or perceptual distortions (appearance of
change in shape or size); cognitive symptoms, such as loss of language
or other cognitive domains or dysmnesia (altered memories), such as
déjà vu or jamais vu; strong emotional symptoms (anxiety, elation, fear).
Usually little or no pallor
Vocalization at onset of generalized convulsion (GC)
Apnoea
Cyanosis associated with GC
Stertorous breathing
Tongue biting
Postictal amnesia—paramedical staff present when patient
‘comes round’, or patient ‘comes round’ in hospital (although he
walked to the ambulance)
Table 16.2 Headaches: points to consider in the history
WWW.BOOKBAZ.IR
https://t.me/med1917
Aspects of history Feature Diagnosis
Location of pain Focal; retro- orbital or supra- orbital Migraine
Laterality Unilateral Migraine, trigeminal autonomic cephalgias
Onset and chronicity New, explosive onset and severe
Duration and
frequency of attacks
Migrainous
symptoms
Cranial autonomic
symptoms
Features of CSF
dysregulation
Trigeminal autonomic cephalgias (cluster
headache, paroxysmal hemicranias, SUNCT,
hemicrania continua)
Retro- orbital lesion
Facial (lower two trigeminal divisions) or dental;
Trigeminal neuralgia
severe and lancinating
Occipital Chiari malformation
Intracranial hypotension
Occipital neuralgia
Cervical spondylosis
Focal over frontal or maxillary sinuses; often with
Sinusitis
tenderness
Temporal; with scalp tenderness Giant cell arteritis
Generalized Migraine, tension- type headache
Subarachnoid haemorrhage
New, acute or subacute onset
Sporadic over years
Bouts lasting days or weeks
Meningitis, cerebral abscess, encephalitis
Migraine
Migraine
Cluster headache
Trigeminal neuralgia
Periodicity: diurnal (attacks at specific times or the day)
Cluster headache
or circannual (bouts at particular times of the year)
Seconds (recurrent) Trigeminal neuralgia
5 to 300 seconds (multiple per day) SUNCT
2 to 30 minutes (usually 5 or more daily) Paroxysmal hemicranias
15 minutes to 3 hours (up to 8 per day) Cluster headache
Hours to days Migraine
Tension headache
Nausea or vomiting
Migraine
Photophobia (sensitivity to light)
Phonophobia (sensitivity to noise)
Osmophobia (sensitivity to smell)
Motion sensitivity
Aura: visual, including photopsia (bright spots and
flashes) or fortification (appearance of zigzag lines)
or scotoma or other visual loss; sensory symptoms
(usually positive) such as tingling or ‘pins and
needles’); and speech or language
Brainstem aura: such as dysarthria, vertigo, diplopia,
ataxia or decreased conscious level.
Conjunctival injection (‘bloodshot’ eyes),
lachrymation (tears), ptosis, nasal congestion,
rhinorrhea (running nostril), eyelid oedema, facial
sweating, miosis (small asymmetric pupil)
Can occur in migraine
Unilateral autonomic symptoms are characteristic
of trigeminal autonomic cephalgias (cluster
headache, paroxysmal hemicranias, SUNCT or
hemicrania continua)
High- pressure symptoms: orthostatic (worse
on lying flat) or diurnal (worse at night or early
morning) variation; exacerbation with Valsalva
(coughing, sneezing, straining, etc.); transient visual
obscurations; or pulsatile tinnitus
Low- pressure symptoms: orthostatic (worse on sitting
or standing) or diurnal (deteriorate as day progresses)
Craniocervical abnormality (such as Chiari
malformation)
Idiopathic intracranial hypertension (associated
with papilloedema and typical body habitus)
Intracranial lesion
Spontaneous CSF leak
Post-lumbar puncture or epidural
Continued
324
https://t.me/med1917
16
Nervous system
Table 16.2 Headaches: points to consider in the history—cont’d
Aspects of history Feature Diagnosis
Situational
headaches
Exacerbating or
relieving factors
General health Systemic neoplasia Metastases
Features of giant
cell arteritis
Important to
specifically consider
in any patient over
60 years of age
CSF, cerebrospinal fluid; SAH, subarachnoid hemorrhage; SUNCT, short- lasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing (a rare
disorder).
Exertion Benign exertional headache
Exacerbates migraine
Orgasm Benign coital headache
SAH should be excluded after single severe episode
Sleep onset Hypnic headache
Migraine
Cluster headache; so called ‘alarm clock
headache’, wakes at same time every night.
Provoked by alcohol Migraine
Cluster headache
Menstrual association and other hormonal aspects
(better or worse during pregnancy; after menopause)
Food precipitants Migraine
Facial touching or movement Trigeminal neuralgia
Body habitus (increased body mass index) Idiopathic intracranial hypertension
Amaurosis fugax (transient monocular visual loss)
Jaw claudication (pain on chewing)
Scalp tenderness
Polymyalgia and weight loss
Migraine
Obstructive sleep apnoea
Giant cell arteritis
cerebellum. A clear- cut description of a spinning feeling usually signifies true vertigo. Patients are more likely
to complain of dizziness or giddiness than vertigo. Both
dizziness and giddiness mean different things to different patients, including vertigo, oscillopsia (a visual sensation that stationary objects are swaying back and forth),
lightheadedness, loss of balance or even sometimes
headache. It is always important to establish whether
a patient with vertigo has positional vertigo. Enquiring
whether the patient’s symptom is provoked by sitting
from a lying position or standing from a sitting position
will not distinguish vertigo from postural hypotension
or ataxia, because all give rise to symptoms on rising.
Symptoms brought on by lying down or turning over
in bed or looking up at a high shelf or the sky more
certainly signify real positional vertigo. It is not uncommon for patients with loss of balance to complain of
dizziness; such patients will spontaneously comment
that they feel secure sitting in a chair but dizzy as soon
as they stand up and move around.
Focal weakness is self- explanatory. Many patients
complain of feeling generally weak when they have no
loss of muscle strength at all. Some patients become
weak without realizing it. Thus, patients with unilateral
or bilateral quadriceps weakness may present with
falls rather than complain of weakness. Patients with
bilateral ankle dorsiflexion weakness may complain of
being off balance or of tripping rather than weakness.
Exertional weakness or worsening of weakness is
characteristic of neuromuscular junction disorders,
but it also occurs in cauda equina compression (spinal
canal stenosis), spinal cord compression (cervical
spondylotic myelopathy) and in multiple sclerosis and
sometimes other disorders, so it is not specific but can
be diagnostically helpful and so should be asked about.
Sensory symptoms may be negative (a reduction or
absence of normal sensation) or positive (an abnormal sensation which is felt, e.g. buzzing, tingling, ‘pins
and needles’, pain). In ordinary usage, the word numb
would seem to be unambiguous, but some patients
who are weak without sensory loss refer to numbness
(particularly in Bell’s palsy) and, conversely, patients
with sensory migraine auras may be misdiagnosed as
having hemiplegic migraine because of their impression
of paralysis even though they can move the affected
limbs. Patients who seem imprecise have some justification; the Shorter Oxford Dictionary defines numb
as ‘deprived of feeling, or of the power of movement’
so it is important to clarify exactly what the patient is
describing. As a rule, transient ischaemic attacks that
involve the parietal cortex give rise to brief negative
sensory symptoms. Conversely, focal sensory seizures
are characterized by positive sensory symptoms.
Most organic neurological disorders that give rise
to sensory symptoms involve structural or functional damage to nerves somewhere, whether it be
in peripheral nerves, nerve roots, spinal cord or brain.
Hypersensitivity (hyperaesthesia) to all modalities
of sensation is therefore improbable or impossible.
Patients who appear to have very sensitive skin as a
SECTION THREE
WWW.BOOKBAZ.IR
https://t.me/med1917
Nervous system
325
Table 16.3 Nomenclature of cutaneous sensory symptoms
Hypoaesthesia Reduced cutaneous sensation of any
modality
Paraesthesia Spontaneous abnormal sensation
including tingling, pins and needles and
pain
Neuralgia Pain in the distribution of a nerve or nerve
root
Dysaesthesia An abnormal perception of a sensory
stimulus (e.g. touch causes tingling or pain)
Allodynia Pain caused by a stimulus that does not
normally cause pain
Hyperalgesia An abnormally intense perception of a
mildly painful stimulus
Hyperpathia Perseveration, augmentation and, on
occasion, spread of pain
The pain threshold is normal or
sometimes high
The threshold for perceiving pain may be
raised and there may be delay in perceiving
a painful stimulus; once perceived, the pain
is severe and prolonged and may spread
Hyperaesthesia An ambiguous term, best avoided
result of a lesion (e.g. herpes zoster radiculitis) have
combinations of paraesthesia, hypoaesthesia, dysaesthesia, allodynia, hyperalgesia and hyperpathia.
Some of these terms are not without their ambiguities. Table 16.3 provides a definition for each.
Lhermitte’s symptom (often called Lhermitte’s sign)
is a paroxysm of positive sensory symptoms—an electric shock feeling or a shower of paraesthesiae shooting
down the spine and/or into the upper or lower limbs
triggered by neck flexion. It is indicative of a cervical spinal cord lesion, commonly a multiple sclerosis
plaque, although other cord lesions (e.g. spondylotic
cord compression) and even cobalamin (vitamin B12)
deficiency may also produce this symptom.
Neurological examination is poor at identifying and
characterizing disorders of the autonomic nervous system, making it particularly important that autonomic
function (including bladder and bowel control and
sexual function) is addressed in the history.
The neurological examination
Aspects of neurological examination can start from
the moment the patient is first encountered, before
and during the taking of the history, such as noting an
abnormality of gait, difficulties with speech, parkinsonism or a hyperkinetic movement disorder. There is
no such thing as a comprehensive neurological examination—it would take hours or days. However, too
many patients without neurological symptoms have
no neurological examination at all, which on occasions
proves regrettable. Consider, for instance, the case of a
man who develops areflexic weakness some days after
a hernia operation. How helpful would it be to know
that the reflexes had been normal at the time of preoperative clinical clerking? A suggested minimal neurological examination for non- neurological patients
would be assessments of the binocular visual fields,
the eye movements, the biceps, triceps, knee and
ankle reflexes, the plantar reflexes and fundoscopy.
Most patients attending for a neurological consultation (with problems such as headache or epilepsy)
have no neurological signs. A minimal routine neurological examination for such patients should include
assessments of vision, the cranial nerves, motor and
sensory examination and examination of gait. Bear in
mind that many patients with early cognitive impairment are adept at concealing it, so that without probing it can be missed.
For most patients, it is best to be systematic with
regard to neurological examination, adhering to a
routine well rehearsed by the examiner and familiar
to those with whom the examiner will communicate.
Thus, even if the patient’s problem is foot drop, it
is entirely valid to start with examination of cranial
nerves but sensible to explain to the patient that you
are going to start at the top and work down. Certain
situations require flexibility; patients with any degree
of impairment of consciousness need assessment of
their delirium or coma from the outset. In patients
presenting with cognitive impairment, it is best to
start the examination with cognitive assessment.
It is important in all neurological patients to pay
attention to and document mobility and, in patients
presenting with a gait disorder, it is appropriate to
examine the gait first. For most other patients, an
appropriate order of examination is cranial nerves,
speech if necessary, motor system, sensory system
and gait, followed by cognitive testing if relevant.
Cranial nerve examination
Examination of the 12 cranial nerves actually involves
an assessment of much more than just the nerves
and nuclei, particularly with respect to the sensory
visual system and eye movements. The naming and
numbering of cranial nerves and their nuclei is in some
measure idiosyncratic and confusing; for example,
there is no olfactory nerve as such and the eighth
cranial nerve is actually two nerves, as is the seventh.
Within the brainstem, trigeminal sensory nuclei
receive fibres not just from the fifth cranial nerve but
also from the seventh, ninth and tenth nerves.
The olfactory (I) nerves
Olfactory receptor cells are bipolar sensory neurons
situated under the nasal epithelium. Their central
axons project in numerous bundles, not as a discrete
nerve, up through the cribriform plate of the skull
into the olfactory bulb on the inferior surface of the
frontal lobe. These project via the olfactory tract to
parts of the temporal lobe and frontal lobe.
326
5
Visual field of
Visual field of
https://t.me/med1917
16
Nervous system
Examination of the olfactory nerves
For ordinary clinical purposes, olfaction is tested using
a small number of bottles containing either a fragrant
or pungent smelling substance, such as lemon, clove
or asafoetida. More detailed odour identification can
be performed using specialist testing kits, such as the
University of Pennsylvania Smell Identification Test
(UPSIT), in which the patient scratches microencapsulated odorant in strips and identifies the smell. Each
nostril should be tested separately. A necessary precondition is that a rhinological disorder does not preclude
the test. Ideally, the patient should identify the smell
rather than just report that it can be smelt. There is little value in routinely testing olfaction; it is uncommon
to detect an abnormality and even less common for an
abnormality to contribute to a diagnosis. A subfrontal
tumour, such as a meningioma, may cause unilateral
anosmia, but other features of the history and examination will mandate the imaging, which should establish that diagnosis. Subfrontal meningiomas can cause
bilateral anosmia, so imaging is indicated in a patient
presenting just with anosmia unless another cause is
clearly evident. Olfactory nerve fibres passing through
the cribriform plate are not uncommonly sheared as a
result of head injury, frequently leading to permanent
bilateral anosmia. Anosmia is commonly neurodegenerative, occurring particularly in Lewy body disease, so
its presence in a patient with parkinsonism increases
the likelihood that the patient has idiopathic (Lewy
body) Parkinson’s disease. Endocrinologists test olfaction when Kallman’s syndrome is suspected.
The optic (II) nerves (see also Chapter 21)
The optic nerve runs from the back of the globe of the
eye to the apex of the orbit and into the skull through
the optic canal to the optic chiasm, where it is joined
by the optic nerve from the other eye. Directly above
the optic chiasm is the hypothalamus. Directly below
is the pituitary gland. The pituitary stalk runs from the
hypothalamus to the pituitary gland just behind the
optic chiasm, between the optic tracts. Sensory afferents from all points of the retina run in the nerve- fibre
layer on the inner surface of the retina to enter the optic
nerve at the optic disc. Fibres from the temporal retina
(nasal visual half- field) are placed laterally, whereas
those from the nasal retina (temporal visual half- field)
are medial. Fibres from the upper half of the retina run
in the upper half of the optic nerve. At the optic chiasm, fibres from the nasal half of the retina (temporal
visual half- field) cross (decussate) to the contralateral
optic tract, whereas the fibres from the temporal half
of the retina do not cross, but proceed posteriorly into
the ipsilateral optic tract (Fig. 16.1). Starting within the
chiasm and continuing further posteriorly within the
optic tract, fibres which convey matching information
left eye
3a
4
7
Anatomy
Figure 16.1 A diagram of the sensory visual pathways.
lesion. 2. Optic chiasm lesion (bitemporal hemianopia). Lesions superior to the chiasm, for example craniopharyngioma, affecting upper chiasm
fibres may cause bitemporal inferior quandrantanopia, whereas lesions inferior to the chiasm, for example the pituitary, may result in bitemporal
superior quadrantanopia. 3a or 3b. Uniocular nasal hemianopia (rare). 3a plus 3b. Binasal hemianopia (very rare). 4. Optic tract lesion
(incongruous homonymous hemianopia). 5. Visual radiation (homonymous quadrantanopia or hemianopia). Inferior optic radiation (temporal
pathway or Meyer’s loop) results in homonymous superior quadrantanopia, whereas superior optic radiation (parietal pathway) results in
homonymous inferior quadrantanopia. 6a. Occipital cortex lesion sparing the occipital pole (homonymous hemianopia with macular sparing). 6b.
Occipital pole lesion (homonymous paracentral hemiscotoma). 7. A bilateral occipital cortex lesion (homonymous altitudinal hemianopia).
right eye
2
6
1
3b
Hemifield
Macula
Lens
Retina
Optic nerves
Optic chiasm
Optic tract
Lateral geniculate body
Optic radiation
Peripheral vision
Occipital cortex
Macular vision
Sites of lesions and the visual field defects they produce are shown. 1. Optic nerve
Left
Visual fields
Right
1
2
3a
2 + 3b
4
5
6a
6b
7
SECTION THREE
WWW.BOOKBAZ.IR
https://t.me/med1917
Nervous system
327
from each eye (i.e. homonymous fibres, representing
equivalent parts in the temporal retina for one eye,
nasal retina for the other eye) become aligned with
each other. Thus, each optic nerve conveys information
from its respective eye, but every part of the sensory
visual system behind the optic chiasm on each side
deals with vision for the contralateral binocular visual
half- field.
The majority of optic tract fibres pass, via the
lateral geniculate nucleus, to the occipital cortex.
The lower part of the visual radiation transmits visual
information from the inferior temporal retina of the
ipsilateral eye and inferior nasal retina of the other
eye. A few optic tract fibres pass via the superior
colliculus to the midbrain to mediate the afferent
limb of the pupillary light reflex via connections to
the Edinger–Westphal nuclei.
Visual acuity and colour vision
Visual acuity is of neurological as well as ophthalmological importance, because optic nerve disease
may lead to any degree of loss of acuity. For ordinary
clinical neurological purposes, the acuities measured
using the Snellen chart are adequate. Severe loss of
acuity (<6/60, the top letter on the Snellen chart)
is documented as the ability to count fingers at 1
metre, ability to perceive hand movements, perception of light only and no perception of light.
Acquired unilateral loss of colour vision is a characteristic feature of optic neuropathy, and loss of
colour vision can occur when visual acuity is well
preserved. Thus, testing colour vision using Ishihara
plates may be a sensitive bedside test for mild optic
neuropathy.
Visual fields
Assessment of the visual fields is a key part of the
neurological examination and need not take very
long to perform. Field defects of importance are
commonly missed because they have not been
looked for adequately. Increasingly, opticians measure visual fields, but it cannot always be assumed
that a recent ophthalmological assessment will have
included the visual fields.
Visual field defects in one eye indicate a retinal or
optic nerve disorder. They may affect any part of the
field of the affected eye or nerve. Lesions at the optic chiasm or lesions behind the chiasm in the optic
tracts, visual radiations or occipital cortex give rise to
visual field defects affecting both eyes. Unilateral retrochiasmal lesions give rise to field defects affecting
the contralateral binocular half- field, and the defects
are homonymous (i.e. they affect equivalent parts of
the temporal half- field of one eye and the nasal halffield of the other). Congruity refers to the extent to
which the defects in the two half- fields match each
other exactly. A congruous homonymous hemianopia indicates a lesion in the occipital cortex, whereas
a non- congruous homonymous hemianopia is more
likely to occur with an optic tract lesion.
When ophthalmologists do visual field testing,
they tend to do Goldmann perimetry or to obtain
automated Humphrey fields. The results of these
tests are very useful, but in the clinic or on the ward,
neurologists and general physicians test visual fields
by simple confrontation field testing, comparing the
patient’s fields with their own, assuming their own
to be normal.
Examination of the visual fields
It is best to start by testing the binocular visual fields
(i.e. the patient and examiner both have both eyes
open). Start by asking the patient to look at your face.
Ensure that he avoids the common temptation to
look to either side. Hold your hands up one on each
side at face level, with your hands about 1 m apart
and ask the patient whether he can see both hands.
This simple test will detect a dense homonymous
hemianopia. Next ask the patient to look into your
eyes. Switch from hands held up to index fingers held
up and move them up so that they are situated in the
right and left superior quadrants of vision. Wiggle one
of your fingers and instruct the patient to point to
the finger he thinks is moving. Getting the patient to
right or left finger that is moving; many patients will
muddle left and right in this situation. First wiggle one
finger, then the other, to check the integrity of the
superior quadrants. Failure of the patient to see one of
the fingers wiggling suggests a homonymous quadrantanopia. If that happens, carry on wiggling the finger
that has not been registered by the patient and move
it first across the midline to make sure that it becomes
visible at the midline and then go back and do the
same, this time moving the finger down into the inferior quadrant, where the finger will be visible if the
patient has a quadrantanopia or remain unseen if the
patient has a homonymous hemianopia. If the patient
sees each finger wiggling consecutively in each of the
upper quadrants, then wiggle both fingers simultaneously and ask the patient what is happening. If the
patient only sees the wiggling of the finger on one
side consistently, then he has visual inattention—an
occipitotemporal or occipitoparietal disorder. Having tested the superior quadrants, move down to the
inferior quadrants to test them in the same way. With
a cooperative patient, all of this takes only a matter
of seconds. The technique described will not detect a
bitemporal hemianopia, optic nerve lesions or retinal
disorders; these require testing of the field for each
eye separately.
The best way to test the monocular visual fields at
the bedside is to use a pin with a bright red pinhead of
about 5–8 mm diameter. The patient needs to be positioned such that light is not shining from behind the
examiner into the patient’s eyes, so as to interfere with
his ability to see the colour of the pinhead. The margin
of the field is defined by the points at which perception
of the colour of the pinhead changes from black to red.
Ask the patient to cover one eye with the palm of his
Соседние файлы в папке Библиотека им академика М.И. Перельмана