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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2612_Библиотеки_им_академика_М_И_Перельмана
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I think, therefore I am
https://t.me/med1917
It is the brain, more than any other organ, that marks Homo sapiens apart from
other animals. Our ability to be self- aware, to think, and to reason has formed
the basis of scientific inquiry and philosophical speculation for millennia, as we
attempt to rationalize and define this cognitive capability. What is the mind?
Less tangible than other aspects of our being, throughout time humans have
looked to explanations from philosophy, folklore, religion, and now science. The
concept of the sense of self and being that defines us all— whether it be called
the ego, nous, or the soul— remains intriguing yet elusive to explain. Aristotle
held that the psyche (Greek: ψυχή= soul) was not separate to its housing body,
as one could not exist without the other. This view was directly contradicted by
17
th- century French philosopher René Descartes. He proposed the theory of
the
‘mind– body dualism’ in which the mind, located in the pineal gland, is an entirely
separate entity to the material being, and controls the avatar of the physical body
like a puppeteer.
Thes e conflicting view points well illustrate the s pectrum of neurol ogical dis-
ease and its blurred boundaries with psychiatry and psychology. Jean Martin
1825– 1893
Charcot (
more interested in this crossover than neuronal dysfunction: he spent two decades
of his career studying hysteria in Paris, initially attributing symptoms of crying,
fainting, and temporary blindness to an organic, inherited cause, before revising
his view in later life to conclude that this was a psychological disease. His controversial work in this field inspired his student Sigmund Freud’s psychoanalytical
theories, and illustrated the very real power of the conscious, or subconscious, to
produce physical symptoms, a phenomenon familiar to all physicians. Perhaps reflecting our frustration with this challenging area as much as his limited success,
we remember Charcot for his more tangible outputs, for example, in giving the inaugural description of, among other things, multiple sclerosis, Parkinson’s disease,
amyotrophic lateral sclerosis (
his eponymous misshapen joint resulting from proprioceptive loss.
However, both Aristotle and Charcot would have surely agreed with Descartes’
proposition of ‘cogito ergo sum’: I think, therefore I am. Whether mind and brain
are dual or one, they are inextricably linked and the very nature of awareness
proves its existence.
), often credited as the father of neurology, appeared to be
ALS
), Charcot– Marie– Tooth disease, and of course
441
10 Neurology
10 Neurology
Where is the lesion?
UMN
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442
This is an important first question to ask and depends on recognizing characteristic
patterns of cognitive, cranial nerve, motor, and sensory deficits. Locating a focal lesion
can be aided by features such as asymmetry (eg one pupil dilated, one upgoing plantar
response) or a spinal level (eects may be symmetrical below the lesion).
sometimes there is no single lesion, rather, a general insult causing a falsely localizing
sign, eg abducens nerve palsy in
are: trauma, encephalitis, anoxia, poisoning, or post- ictal states.
Motor deficits Establish if the pattern is consistent with an upper (UMN) or a lower
motor neuron (
Lesions are caused by damage anywhere along the corticospinal (= pyramidal)
LMN) lesion (table
tracts: motor pathways from the precentral gyrus to the anterior horn cells in the cord
(via the internal capsule and brainstem).
before spasticity and hyperreflexia develop.
where from the anterior horn cells distally, including the nerve roots, plexuses, and peripheral nerves.
p
506
(
The chi ef dierential for
)— but unlike
LMN
reflexes (or lost late), and have no sensory component.
Mixed
LMN
and
UMN
signs Can occur, eg in
Table 10.
1
Examination findings in upper versus lower motor neuron lesions
Exam Upper motor neuron Lower motor neuron
Inspection
Tone
Power
Reflexes
Plantars
Muscle wasting less prominent (disuse
atrophy may be present)
Hypertonia/ spasticity: Vel ocity depe nden t,
ie the faster you move the patient’s
muscle, the greater the resistance, until it
finally gives way (like a ‘clasp- knife’)
Weakness aects muscle groups,
typically in a ‘pyramidal’ pattern: in
the arm, extensors are predominantly
aected; in the leg, flexors are weaker.
Disability is disproportionate to the
weakness (spasticity adds to it)
Hyperreflexia: reflexes are brisk below
the level of the lesion, ± clonus (elicited by
rapid ly dorsiflexi ng the fo ot;
downward beats of the foot are normal)
Plantars are extensor (+ ve Babinski sign)
Sensory deficits It is important to test individual modalities and remember quirks
of normal wiring: correctly interpreted, the distribution of sensory loss and the modality involved (pain,
confidence in localizing the lesion. Pain and
peripheral nerves and the anterolateral (spinothalamic) tracts in the contralateral
cord and brainstem (
fibres in peripheral nerves and the ipsilateral dorsal columns of the cord.
Also ask
What is the lesion? Are the cells diseased, dysfunctional, disconnected (after a
stroke), or under- or overexcited (migraine; epilepsy)? Is there loss of a specific type
of nerve cell, as in
MND
Why? Is there a systemic disease causing the neurology? Eg atrial fibrillation
allowing an embolus to form, causing an infarct. Do a full systems examination
and always beware the irregularly irregular pulse.
1
Most of the fibres of the corticospinal (= pyramidal) tract decussate at the medullary pyramids, hence the
name and the contralateral nature of symptoms. Extrapyramidal denotes damage to the basal ganglia and
presents as Parkinsonism (see
2
Whereas with rigidity, tone is not velocity dependent but constant throughout the range of movement.
Note that
ICP.
Other generalized causes of specific local eects
10.1
), then determine the level (table
1,2
UMN
lesions can mimic
LMN
Lesions are caused by damage any-
LMN
weakness is a primary muscle disease
10.2
).
LMN
lesions acutely
weakness these typically exhibit symmetrical loss, with normal
MND
,
B
, taboparesis (p
12
Muscle wasting ± fasciculation
(involuntary twitching)
Hypotonia/ flaccidity: the
limb feels soft and floppy,
providing little resistance to
2
passive stretch
Wea knes s aects individual
muscles (eg weakness of
dorsiflexors in foot drop).
The functional disability is
proportionate to the weakness
elicited on examination
Hyporeflexia: reflexes are
≤
3
rhythmic,
T
°, touch, vibration, joint- position sense) will increase your
p
512
), whereas joint- position and vibration sense travel in large
T
reduced (or absent) at the
level of the lesion
Plantars are flexor/ absent
° sensations travel along small fibres in
or suba cute comb ined dege nerat ion of th e cord (
p
464
, p
490
).
462
).
B
, p
330
12
)?
Table 10.
NMJ
https://t.me/med1917
Level of
lesion
Cortex
Internal
capsule
Brainstem
Spinal
cord
Anterior
horn cell
Peripheral
nerve
Muscle
2
From findings to neuroanatomy: localizing the lesion
U/ L Signs
May cause a particularly localized problem with, eg hand or foot
UMN
movements, with normal or even tone— but reflexes more
proximally in the arm or leg will point to this being an
LMN
lesion. Sensory loss may be confined to discriminative
than
functions, eg stereognosis and two- point discrimination, and aphasia,
visual field deficits, gaze deviation, and neglect may coexist (
Contralateral hemiparesis alone, or with generalized contralateral
UMN
sensory loss. Lesions of the genu aect bulbar function
UMN
A cranial nerve palsy (
III– XII
) contralateral to a hemiplegia
implicates the brainstem on the side of the cranial nerve palsy.
Lateral brainstem lesions show both dissociated and crossed
sensory loss with pain and
to the lesion, and contralateral arm and leg sensory loss
Parap aresis (both l egs) o r quad ripares is/ tetraplegia (all limbs).
UMN
A motor and reflex level (power is unaected above the lesion,
LMN
signs at the level o f the lesio n, and
with
lesion) suggests a cord lesion. A sensory level is the hallmark (albeit
T
° loss on the side of the face ipsilateral
a rather unreliable one)— ie decreased sensation below the level of
the lesion with normal sensation above. Hemi- cord lesions cause
a Brown- Séquard syndrome: ipsilateral
(corticospinal tract), ipsilateral dorsal column loss, and contralateral
spinothalamic loss; caused by trauma, mass lesions, disc herniation,
or myelitis. Dissociated sensory loss may oc cur, eg in cervical cord
lesions— loss of fine touch and proprioception without loss of pain and
temperature (or vice versa, eg syringomyelia,
LMN
Distal weakness without sensory changes (p
Most cause distal weakness, eg foot- drop; weak hand (note:
LMN
although Guillain– Barré syndrome typically presents as distal
weakness that ascends over time, some atypical forms of Guillain–
Barré syndrome may present with proximal weakness due to nerve
root involvement). Sensory loss is typically worse distally (may
involve all sensory modalities or be selective, depending on nerve
fibre size involved). Involvement of a single nerve (mononeuropathy)
occurs with trauma or entrapment (carpal tunnel,
involvement of several nerves (mononeuritis multiplex) is seen, eg
DM
or vasculitis. Sensory loss from individual nerve lesions will
in
follow anatomical territories (dermatomes,
more sharply defined than those of root lesions
LMN
Fatiguable weakness without sensory changes (p
NA
Gradual- onset symmetrical weakness ± pain (p
UMN
signs below the
UMN
signs below the lesion
p
512
; or cord tumours)
502
)
p
497
p
450
), which are usually
508
)
506
)
UMN
);
rather
p
495
443
)
10 Neurology
Muscle weakness grading (
• Grade
0
No muscle contraction • Grade 3 Active movement against gravity
• Grade
1
Flicker of contraction • Grade 4 Active movement against resistance
• Grade
2
Some active movement • Grade 5 Normal power (allowing for age)
It should be noted that this is an ordinal, not a ratio scale, so the categories do
not represent equal increments of strength. Grade
4
+ denote movement against slight, moderate, and stronger resistance; avoid
fudging descriptions— ‘strength
myopathy. It is better to document ‘poor eort’ and the maximum grade for each
muscle tested.
although sequential grading can help document improvement.
Distribution of weakness tells us more than grade of weakness,
MRC
classification)
4
covers a big range: 4−, 4, and
4/ 5
throughout’ suggests a mild quadriparesis or
10 Neurology
Drugs and the nervous system
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444
The brain is a gland that secretes both thoughts and molecules: both products are
modulated by neurotransmitter systems. Some target sites for drugs:
1
Precursor of the transmitter (eg levodopa).
2
Interference with the storage of transmitter in vesicles within the pre- synaptic
neuron (eg tetrabenazine).
3
Binding to the post- synaptic receptor site (eg bromocriptine).
4
Binding to the receptor- modulating site (eg benzodiazepines).
5
Interference with the breakdown of neurotransmitter within the synaptic cleft
(eg acetylcholinesterase inhibitors; monoamine oxidase inhibitors—
6
Reduce reuptake of transmitter from synaptic cleft into pre- synaptic cell (eg
selective serotonin reuptake inhibitors—
noradrenaline reuptake inhibitors—
7
Binding to pre- synaptic autoreceptors (eg pindolol, a - blocker with partial
5HT
auto receptor antagonist eects, can be used to augment antidepressant
SSRI
S, eg fluoxetine; or serotonin and
SNRI
S, eg mirtazapine).
therapy).
Important neurotransmitters (and some associated drugs) are listed in
Storms on the sea of neurotransmission
The complex and subtle mixture of chemicals that bathes our hundreds of trillions
of synapses has been likened to a ‘sea’ of neurotransmitters. If so, it is surely a
seascape of exquisite beauty, no matter how disturbed cognition may become by
the storms that whip the waves on the surface. A well- chosen prescription may
oer a lifeboat from such storms, but before prescribing any drug that modulates neurotransmission, consider that you are about to release a blunt and poorly
understood force into a delicate environment.
be able to pass through the blood– brain barrier to have an eect.
quences of any sedative eects may be severe.
SE
(eg tardive dyskinesia with neuroleptic drugs). • Most drugs aect many
term
neurotransmitters, increasing therapeutic scope (and uncertainty), eg risperidone
D
,
5HT
(blocks
more important pharmacological eects resulting in clinically important interactions with drugs aecting, eg hepatic metabolism.
may have many eects, eg dopaminergic neurons go awry in Parkinson’s disease,
, 1 and 2 receptors). • Metabolites of drugs may have equal or
2
2
• The drug (or a metabolite) must
• There will be short- and long-
• One neurotransmitter
schizophrenia, and addiction to drugs and gambling, by aecting motor control,
motivation, eort, reward, analgesia, stress, learning, attention, and cognition.
MAOI
S).
table
10.3
• The conse-
.
Table 10.
HT
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3
Major neurotransmitters and associated drugs
Drugs increasing activity (≈ agonists) Drugs decreasing activity (≈ antagonists)
Acts on receptors
Dopamine
Pramipexole, ropinirole, levodopa,
apomorphine (Parkinson’s*)
Cabergoline, bromocriptine
(hyperprolactinaemia; acromegaly)
Serotonin (5- hydroxytryptamine;
Lithium (mood stabilizer)
Sumatriptan (migraine)
Buspirone (partial agonist; anxiety)
Fluoxetine, sertraline (reuptake
D
; aects mood and reward- seeking behaviour
1– 5
Chlorpromazine (schizophrenia,
Metoclopramide (nausea)
Inhibition of dopamine signalling may lead to
drug induced parkinsonism
5
) Many receptor types
5HT
; multiple eects
1– 7
Ondansetron (nausea)
Mirtazapine (depression)
Olanzapine, clozapine (schizophrenia)
OHCS
p
704
inhibitors; depression)
Amino acids Glutamate and aspartate act as excitatory transmitters on
NMDA
receptors— relevant in epilepsy and
non-
GABA
) is mostly inhibitory
(
Gabapentin, valproate (
epilepsy and neuropathic pain)
Benzodiazepines (
sedation)
GABA
Baclofen (
GABA
Alcohol (
GABA
GABA
agonists;
agonists; spasticity)
†
agonist)
agonists;
CNS
ischaemia. - aminobutyric acid
Memantine (glutamate antagonist;
dementia)
Lamotrigine, topiramate (glutamate
antagonists, alongside
and other eects; epilepsy, bipolar disorder,
migraine)
NMDA
NA
channel blocking
and
Acetylcholine Multiple receptors classed into muscarinic and nicotinic types.
Peripheral agonists used in glaucoma (pilocarpine); myasthenia (anticholinesterases).
Peripheral antagonists used in asthma (ipratropium); incontinence; to dry secretions
pre- op; to dilate pupils; to heart rate (atropine). Centrally acting drugs include:
Donepezil, galantamine, rivastigmine
(acetylcholinesterase inhibitors;
dementia)
Histamine and purines (eg
ATP
Procyclidine, trihexyphenidyl (drug- induced
parkinsonism)
)
Cyclizine (antihistamine; nausea)
Purinergic receptor blockers (emerging role
in chronic pain)
Neuropeptides Multiple and growing list; includes opioids and substance
Exogenous opioids (wide- ranging analgesic and mood- related eects)
Aprepitant (chemotherapy- related nausea
by blocking substance
Noradrenaline, adrenaline (= norepinephrine, epinephrine) 4 receptor types:
. Noradrenaline is more specific for - receptors but both transmitters aect all
1– 2
receptors. In the periphery, - receptors drive arteriolar vasoconstriction and pupillary
stimulation leads to pulse and myocardial contractility; 2 stimulation leads
dilation;
1
to bronchodi latation, uterine relaxation, and arteriolar vasodilation. Centrally acting
P
receptors)
P
1– 2
drugs include:
Clonidine (refractory hypertension)
Tricyclic antidepressants and
venlafaxine (
reuptake inhibitors
MAOI
* Agonism at
logical gambling or hobbying, and disorders of impulse control in people having no history of these.
†
In chronic alcohol use,
maintain
5HT
and noradrenaline
;
S
GABA
depression)
D
receptor agonists may cause pathological behavioural patterns, eg hypersexuality, patho-
3
GABA
signalling after alcohol withdrawal.
receptors are downregulated; acamprosate, used in alcoholism, may help to
445
)
10 Neurology
,
10 Neurology
Cerebral blood supply
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446
Knowledge of the anatomy of the arterial supply of the brain helps diagnosis and
management of cerebrovascular disease (
of brain that correlates with a patient’s symptoms and identify the aected artery.
The circle of Willis (fig
the three arteries that supply the brain with blood: the internal carotids (anteriorly)
and the basilar artery (posteriorly, formed by the joining of the vertebral arteries,
which supply the brainstem). This arrangement may compensate for the eects of
occlusion of a feeder vessel by allowing supply from unaected vessels; however,
the anatomy of the circle of Willis is variable and in many people it does not provide
much protection.
Anterior circulation The internal carotid arteries supply the majority of blood to
the anterior two- thirds of the cerebral hemispheres and the basal ganglia (via the
lenticulostriate arteries). At worst, internal carotid artery occlusion causes fatal
total infarction of these areas. More often, the picture is like middle cerebral artery
occlusion. The
supply the lateral part of each hemisphere. Occlusion may cause contralateral hemiparesis, hemisensory loss (esp. face and arm), contralateral homonymous hemianopia
due to involvement of the optic radiation, cognitive change including dysphasia with
dominant hemisphere lesions, and visuospatial disturbance (eg cannot dress; gets
lost) with non- dominant lesions. The
branches of the internal carotids, supply the frontal and medial part of the cerebrum.
Occlusion may cause a weak, numb contralateral leg ± similar, if milder, arm symptoms (unusually, shoulder much weaker than hand). The face is spared. Bilateral infarction is a rare cause of paraplegia and an even rarer cause of akinetic mutism.
Posterior (vertebrobasilar) circulation Supplies the cerebellum, brainstem, thal-
amus, and occipital lobes; occlusion causes signs relating to any or all: hemianopia;
cortical blindness; diplopia; vertigo; nystagmus; ataxia; dysarthria; dysphasia; hemi-
or quadriplegia; unilateral or bilateral sensory symptoms; hiccups; coma. In
the basilar artery divides into the two
that supply the occipital lobes, inferior temporal lobes, and the thalamus. Occlusion
gives contralateral homonymous hemianopia (often with macular sparing), ± nonlocalizing symptoms such as disorientation, confusion, and memory loss. In
a fetal origin is present, in which the bulk of the blood flow to the posterior cerebral artery comes from the anterior circulation, via the posterior communicating
artery. Infarctions of the brainstem can produce various syndromes, eg lateral
medullary syndrome, in which occlusion of one vertebral artery or the posterior
inferior cerebellar artery causes infarction of the lateral medulla and the inferior
cerebellar surface ( vertigo, vomiting, dysphagia, nystagmus, ipsilateral ataxia,
soft palate paralysis, ipsilateral Horner’s syndrome, and a crossed pattern sensory
loss— analgesia to pin- prick on ipsilateral face and contralateral trunk and limbs).
Locked- in syndrome is caused by damage to the ventral pons due to basilar artery
occlusion. Patients are unable to move, but retain full cognition and awareness,
communicating by blinking, electronic boards, or special computers. Right- to- die
legislation may be invoked... as one suerer blinked: ‘My life is dull, miserable, demeaning, undignified, and intolerable.’ Locked- in syndrome is dierent from other
right- to- die conditions because patients need someone to do the act for them.
Subclavian steal syndrome Subclavian artery stenosis proximal to the origin of
the vertebral artery may cause blood to be stolen by retrograde flow down this
vertebral artery down into the arm, causing brainstem ischaemia typically after
use of the arm. Suspect if the
middle cerebral arteries arise directly from the internal carotids and
10.2
) An anastomotic ring at the base of the brain fed by
BP
pp
466– 75
). Always try to identify the area
anterior cerebral arteries, the other terminal
posterior cerebral arteries (figs
in each arm diers by >20mmHg.
80
10.2– 10.4
20
%,
)
%,
‘Dizzy- plus’ syndromes and arterial events
•
SCA
dizzy.
•
AICA
dizzy and deaf.
•
PICA
dizzy and dysphagic and dysphonic.
Anterior cerebral artery
Internal
car
Optic chiasm
sterior communicating artery
aa
mm
pp
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otid artery
Anterior communicating artery
Middle cerebral artery
447
Superior
cerebellar
artery
Pontine
arteries
Basilar
artery
Vertebral
artery
Anterior
spinal artery
Fig 10.
2
The circle of Willis at the base of the brain. See also figs
Po
Posterior cerebral artery
Anterior inferior
cerebellar artery
Posterior inferior
cerebellar artery (PICA)
10.19, 10.20
(and
10.25
10 Neurology
for veins).
Fig 10.
3
Berry aneurysm at junction of
posterior communicating artery with internal carotid (
p
474
). © Dr D Hamoundi.
Thomas Willis
Thomas Willis (
DM
degree, awarded in
the most loyally royal college in the University. He had a busy life inventing terms
such as ‘neurology’ and ‘reflex’. Not only has his name been given to his famous
1621– 1675
circle, but he was the first to describe myasthenia gravis, whooping cough, and
the sweet taste of diabetic urine. He was the first person (few have followed him)
to know the course of the spinal accessory nerve. He is unusual among Oxford
neurologists in that he developed the practice of giving his lunch away to the
poor. He also espoused iatrochemistry: a theory of medicine according to which
all morbid conditions of the body can be explained by disturbances in the fermentations and eervescences of its humours.
Fig 10.
4
CT of stroke in posterior
cerebral artery territory.
© J Trobe.
) is one of those happy Oxford heroes who hold a bogus
1646
for his Royalist sympathies while at Christ Church,
10 Neurology
Testing peripheral nerves
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448
While there is some anatomical variation between individuals in ascribing par-
tables
10.4– 10.6
ticular nerve roots to muscles,
Dermatomes and sensory nerve roots are shown in
represent a reasonable compromise.
figs
10.5– 10.9
, pp
Remember to test proximal muscle power: ask the patient to sit from lying, to
pull you towards themselves, and to rise from squatting (if reasonably fit).
Observe walking— easy to forget, even if the complaint is of diculty walking!
Don’t be caught out by weakness secondary to musculoskeletal pathology— the
traditional neurological examination relies on the musculoskeletal system being intact. Ruptured tendons and fractures may mimic focal neurological lesions.
Table 10.
4
Assessment of peripheral nerve function in the lower limb
Nerve root Muscle Test by asking the patient to:
Femoral nerve
L1, 2, 3
Iliopsoas (also supplied via
L1, 2
, & 3 spinal nerves)
Flex hip against resistance with knee
flexed and lower leg supported: patient
lies on back
L2, 3, 4
Quadriceps femoris
Extend at knee against resistance. Start
with knee flexed
Obturator nerve
L2, 3, 4
Hip adductors
Adduct leg against resistance
Inferior gluteal nerve
L5, S1, S2
Gluteus maximus Hip extension (‘bury heel into the
couch’)— with knee in extension
Superior gluteal nerve
L4, 5, S1
Gluteus medius and minimus Abduction and internal hip rotation
with leg flexed at hip and knee
Sciatic, common peroneal*, and tibial** nerves
*
L4, 5
*
L5, S1
*
L5, S1
*
L5, S1
*
L5, S1
L5, S1, 2
Tibialis anterior
Extensor digitorum longus
Extensor hallucis longus Dorsiflex hallux against resistance
Peroneus longus and brevis Evert foot against resistance
Extensor digitorum brevis Dorsiflex proximal phalanges of toes
Hamstrings (short head of
biceps femoris is from the
Dorsiflex ankle
Dorsiflex toes against resistance
Flex knee against resistance
common peroneal nerve)
**
**
**
**
L4, 5
S1, 2
L5, S1, 2
S1, 2
Tibialis posterior
Gastrocnemius
Flexor digitorum longus
Small muscles of foot Make the sole of the foot into a cup
Invert plantarflexed foot
Plantarflex ankle or stand on tiptoe
Flex terminal joints of toes
450– 1
.
Table 10.
5
Rapid screening tests for peripheral nerve roots
*
Abduction
Adduction
Flexion
Extension
Flexion
Extension
Shoulder
Elbow
Wrist
Flexion
Fingers
Extension
Abduction
* Wrist movement innervation diers in medial and lateral flexion/ extension, and therefore is a poorer
discriminator of peripheral nerve roots than, eg shoulder abduction
C5
C5– C7
C5– C6
C7
C7–
C7
C8
C7
T1
Flexion
Hip
Adduction
Extension
Knee
8
Flexion
Extension
Dorsiflexion
Ankle
Eversion
Plantarflexion
Toe
Big toe extension
L1– L2
L2–
L5– S1
L5– S1
L3– L4
L4
L5– S1
S1– S2
L5
3
Table 10.
P
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6
Assessment of peripheral nerve function in the upper limb
Nerve root Muscle Test by asking the patient to:
C3, 4
C5, 6, 7
C5, 6
C6, 7, 8
C5, 6
C5, 6
C6, 7, 8
C5, 6
C5, 6
Radial nerve (p
C6, 7, 8
C5, 6
C5, 6
C6, 7
C7, 8
C7, 8
C7, 8
C7, 8
C7, 8
Median nerve (p
C6, 7
C6, 7
C7, 8, T1
C7, 8
C7, 8, T1
C8, T1
C8, T1
C8, T1
Ulnar nerve (p
C7, 8, T1
C7, C8
C8, T1
C8, T1
C8, T1
C8, T1
C8, T1
* Metacarpophalangeal joint flexion may also be more on the aected side as flexor tendons are
recruited— the basis of Froment’s paper sign. Wartenberg’s sign is persistent little finger abduction.
Trapezius Shrug shoulder (via accessory nerve)
Serratus anterior Push arm forward against resistance;
Pectoralis major (P major)
clavicular head
major sternocostal head
Supraspinatus
Infraspinatus
Latissimus dorsi Adduct arm from horizontal position
Biceps Flex supinated forearm
Deltoid
496
)
Triceps Extend elbow against resistance
Brachioradialis Flex elbow with forearm half way be-
Extensor carpi radialis longus Extend wrist to radial side
Supinator Arm by side, resist hand pronation
Extensor digitorum
Extensor carpi ulnaris Extend wrist to ulnar side
Abductor pollicis longus
Extensor pollicis brevis
Extensor pollicis longus
498
)
Pronator teres
Flexor carpi radialis Flex wrist towards radial side
Flexor digitorum superficialis
Flexor digitorum
profundus
I & II
Flexor pollicis longus Resist thumb extension at interphalangeal
Abductor pollicis brevis
Opponens pollicis
1
st lumbrical/ interosseus (median and ulnar nerves)
498
)
Flexor carpi ulnaris Flex wrist to ulnar side; observe tendon
Flexor digitorum profundus
III & IV
Dorsal interossei
Palmar interossei Finger adduction: pull apart a sheet of
Adductor pollicis
Abductor digiti minimi Abduct little finger
Flexor digiti minimi
look for scapula winging (
Adduct arm from above horizontal, and
push it forward
p
507
) if weak
Adduct arm below horizontal
Abduct arm the first
Externally rotate semi- flexed arm, elbow
at side
Abduct arm between
15
°
15
° and 90°
tween pronation and supination
Keep fingers extended at
Abduct thumb at
Extend thumb at
Resist thumb flexion at
90
° to palm
MCP
joint
IP
MCP
joint
joint
Keep arm pronated against resistance
PIP
Resist extension at
imal phalanx fixed by the examiner)
Resist extension at index
index finger
joint (with prox-
DIP
joint of
joint (fix proximal phalanx)
Abduct thumb (nail at
Thumb touches base of
(nail parallel to palm)
Extend
PIP
joint against resistance with
MCP
joint held hyperextended
Resist extension of distal phalanx of 5th
finger while you fix its middle phalanx
Finger abduction: cannot cross the
middle over the index finger (tests index
finger adduction too)
paper held between middle and ring
finger
DIP
joints of both hands; the paper
moves on the weaker side
Adduct thumb (nail at
Flex little finger at
MCP
90
° to palm)
5
th fingertip
*
90
° to palm)
joint
449
10 Neurology
10 Neurology
Dermatomes and peripheral nerves
Fig
10
C
– T2)
https://t.me/med1917
450
Fig 10.
5
The white areas denote terra incognita: considerable inter- individual variation
exists, and no single best option can be given.
Fig 10.
6
Pain in a dermato mal distribution suggests a problem with
a cranial nerve or dorsal root ganglion (radiculopathy)— where the cell
bodies of sensory fibres live. What is
the dermatome? What is the lesion?
p
400
fo r th e an swer .
See
Aim to keep a few key dermatomes up
your sleeve (
5
C3– 4
C6
T1
C6
C7
C8
T4
T10
L1
L2
L5
L5
S1
S2
Clavicles
Lateral arm/ forearm
–
7
Medial side of arm
Thumb
Middle finger
Little finger
Nipples
Umbilicus
Inguinal ligament
Anterior and inner leg
–
3
Medial side of big toe
Posterior and outer leg
, S1–
2
Lateral margin of foot and
little toe
–
4
Perineum
Rough approximations!
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