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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3050_Библиотеки_им_академика_М_И_Перельмана
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290 Neurological observations (IV)
Posterior
Olivospinal
Olivospinal
Lateral tegmentospinal
Lateral tegmentospinal
Lateral corticospinal
Lateral corticospinal
Lateral reticulospinal
Lateral reticulospinal
Ventral vestibulospinal Ve ntral vestibulospinal
Ventral reticulospinal Ventral reticulospinal
Anterior
Ventral corticospinal Ventral corticospinal
(ventral)
Figure 14.3 Superior view of a cross section of the spinal cord sho wing the motor pathways within
the white matter of the cord.
pass down the spinal cord in specic positions within the white matter (Figure 14.3).
The bres enter the anterior grey matter of the cord, where they synapse with other
neurons at all the spinal levels, i.e. from high in the cervical (neck) region to low in the
sacral (pelvic) region.
Lower motor neurons (LMNs) begin with cells in the anterior grey matter of the cord,
and the bres pass via the anterior root of the spinal nerve to the voluntary skeletal mus-
cles of the body. The LMN is therefore part of the peripheral nervous system (PNS), being
a component of the spinal nerves. So, the pyramidal system is two-neuronal, i.e. consist-
ing of a UMN (brain to cord) and an LMN (cord to muscle; Figure 14.1).
The pyramidal system also operates through some of the cranial nerves that control
muscles of the head, face and neck. The corticobulbar tracts (Figure 14.4) begin as neu-
ronal cell bodies in the head and neck areas (lateral areas) of the motor cortex (hence
cortico). These UMN bres pass down to nuclei in the pons and medulla of the brainstem
(note: the pons, part of the brainstem, is called bulbar, i.e. shaped like a bulb). From a
nucleus in the pons, LMN bres become components of the trigeminal nerve (cranial V)
and pass to the muscles of the lower jaw, e.g. for eating. Also from the pons, LMN bres
form part of the facial nerve (cranial VII) and pass to muscles of the face e.g. for facial
expression. Separate medullary nuclei give rise to LMN bres within the glossopharyn-
geal nerve (cranial IX), to pharyngeal muscles, the vagus nerve (cranial X) to muscles of
the pharynx, larynx, oesophagus and soft palate and the spinal accessory nerve (cranial
XI) to the neck muscles.
The extrapyramidal system
This system operates skeletal muscle at the subconscious level, i.e. it controls the auto-
matic aspects of voluntary movement. The main areas of the brain involved are parts of
the brainstem i.e. nuclei of the pons and medulla, which in turn are inuenced by the
basal ganglia, some sensory parts of the cerebral cortex, and parts of the thalamus and
cerebellum, including all their pathways and feedback circuits (Figure14.5).
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IV
V
VII
XI
VI
X
XII
XI
Right cerebral
hemisphere
Motor
cortex
From
midbrain
From
pons
III
V
VI
VII
From
medulla
Neurological observations (IV) 291
Figure 14.4 T he corticobulbar tracts to the cranial nerves. This schematic diagram shows motor
pathways coming from the head and neck area of the right motor cortex (Figure 14.2)
and passing into the brainstem. The cranial nerve nuclei are indicated, showing their
brainstem locations, the corticobulbar input (unilateral or bilateral) and which ones
cross the midline. The left hemisphere (not shown) has a mirror image input.
Some pathways involved are:
1 Primary cells within the cerebral cortex that have bres that end in the red nucleus
within the midbrain, the corticorubral tract. In the red nucleus, secondary cells give
rise to bres that pass down the cord, forming the rubrospinal tract
2 Several nuclei towards the base of the brain are collectively called the basal ganglia
(Figure 14.6). One of these nuclei, the globus pallidus, has primary cells providing
bres that terminate in some areas of the thalamus. From the thalamus, secondary cell
bres feed back to the motor cortex of the cerebrum, i.e. part of the basal ganglia motor
loop (Figures 14.5 and 14.8 and see page 294)
3 Areas of the pons and medulla, known as the reticular formation, have secondary cells
with bres extending down the cord, creating the reticulospinal tract.
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Cerebral cortex
Thalamus
Brainstem
LMN LMN
To right
muscles
To left
muscles
Right
globus
pallidus
Left
globus
pallidus
Red nucleus
Pontine reticular
nucleus
Medullary reticular
nucleus
Medullary
reticulospinal tract
Pontine
reticulospinal tract
Rubrospinal tract
292 Neurological observations (IV)
Figure 14.5 Some extr apyramidal tracts. Pathways of the extrapyramidal system extend from the
cerebral cortex to the red nucleus, and from the red nucleus to the contralateral lower
motor neuron (LMN) in the cord, a pathway called the rubrospinal tract. Another path-
way passes from the globus pallidus to the thalamus with feedback pathways to the
cortex. Other pathways include those from the pontine nucleus to the ipsilateral LMN,
called the pontine reticulospinal tract, and from the medullary reticulospinal nucleus
to the LMN, called the medullary reticulospinal tract.
The basal ganglia and thalamus
The ve nuclei of the basal ganglia (Figure 14.6) have a major inuence on movement,
both facilitatory and inhibitory (Anderson and Kiehn 2004). Facilitatory promotes move-
ment and inhibitory prevents movement. These nuclei have a role in slow, sustained
movements and in maintaining muscle tone (Figure 14.7).
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Neurological observations (IV) 293
Cerebral cortex
Right
Left
Corpus callosum
Lateral
ventricle
Lateral
ventricle
Caudate
nucleus
ThalamusThalamus
Caudate
nucleus
Putamen
GP
ST
ST
GP
Putamen
3
SN
Figure 14.6 Areas that make up the basal ganglia. GP: globus pallidus; SN: substantia nigr a; ST:
subthalamus; 3: third ventricle.
Muscle tone is a state of readiness for contraction, a tension within the muscle that is
essential if the muscle is to function instantly when stimulated. Exercise increases muscle
tone and a lack of exercise causes a loss of tone. Bed rest causes many complications,
including muscle tone loss, i.e. loose, oppy muscles that do not function properly. The
basal ganglia also provides inhibition (or reduction) of excessive muscle tone, and this is
a major role of the substantia nigra (Figure 14.6 and see page 304). Excessive tone causes
muscle stiffness and rigidity, as in Parkinson’s disease (see page 303).
An important inuence over movement is the basal ganglia motor loop (Figure 14.8),
in which the globus pallidus inhibits part of the thalamus (the ventral lateral nucleus,
or VL) during rest. Activation of the motor cortex of the cerebrum switches on another
nucleus of the basal ganglia, the putamen, part of the corpus striatum. The putamen in
turn inhibits the globus pallidus, thus removing the inhibition on the thalamus. Free now
to act, the thalamus has considerable inuence over an area close to the motor cortex, the
supplementary motor area (SMA), which in turn focuses the activity of the main motor
cortex. The loop is complete when the motor cortex activity switches on the mechanism
that focuses that activity (Figure 14.8).
The cerebellum
The cerebellum (Figure 14.9) contributes several aspects of movement, not least of which
are balance and posture.
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Cerebral cortex
Frontal lobe
Motor
Prefrontal cortex
SMA
Parietal
lobe
Sensory
cortex
Area
4
Area
6
Putamen
Thalamus
VL
0
Globus
pallidus
294 Neurological observations (IV)
Line of
A
muscle origin
Loss
of
tone
Contract
B
C
D
Figure 14.7 Muscle tone. (A) Loss of muscle tone: the muscle is soft, loose and oppy, sinking in
response to gravity (i.e. after long period of immobilisation). (B) Normal muscle tone:
the muscle is rm and retains its shape, ready for contraction. (C) Contraction of the
muscle, where the insertion (distal end of the muscle opposite to the origin) moves
towards the origin (proximal end which does not move). (D) Muscle wasting, where
muscle bulk is lost. Excessive muscle tone appears as the opposite of A, i.e. the muscle
is tight and stiff and cannot contract normally.
Figure 14.8 Basal ganglia motor loop. Input to the putamen comes from the frontal cortex, with
less input from the parietal sensory cortex. This activates (+) neurons running from the
putamen to the globus pallidus, which, in turn, then deactivate (−) neurons linking the
globus pallidus with the ventral lateral nucleus of the thalamus (known as VL
0
). These
globus pallidus neurons prevent (i.e. inhibit, shown as −) any feedback from the VL
0
the cerebral cortex. However, deactivation from the putamen has removed this inhibi-
tion, and the VL
0
supplemental motor area (SMA) of area 6 of the motor cortex.
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PONS
Anterior
Lobe
Midbrain
Medulla
Posterior
Lobe
Flocculonodular
Lobe
Neurological observations (IV) 295
Figure 14.9 Section through the cerebellum sho wing the lobes and brain stem (midbrain, pons and
medulla).
The equilibrium of the body requires the centre of gravity (in the mid-lumbar spinal
area) to remain within the base, i.e. the oor area occupied by the two feet. Should the
centre of gravity drift outside the base, the individual will become unstable and will
possibly fall to one side. To prevent this, many minute muscular adjustments are con-
stantly being made to keep the body upright inside the base, correcting any defects in
posture at the same time. These muscular adjustments are constantly changing as the
body moves and the base constantly changes. Muscular contractions are coordinated
by the cerebellum at an unconscious level, but they require sensory feedback to tell
the cerebellum what the second-by-second state of the body’s balance is. This sensory
feedback on balance (known as vestibular stimuli) comes from the semicircular canals
of the inner ear, via the vestibulocochlear nerve (cranial nerve VIII). Additional sensory
information on balance comes from receptors in the joints and muscles called proprio-
ception, and arrives in the brainstem via the spinal cord. Visual information is also used
to assess balance (see vestibulo-ocular reex, Chapter 15). The cerebellum, like the
cerebrum, is divided into left and right hemispheres, both of which communicate with
the rest of the brain entirely via the brainstem. Each cerebellar hemisphere is divided
into three lobes: the occulonodular lobe, the anterior lobe and the posterior lobe
(Figure 14.9).
The vestibular stimuli from both ears arrive at the occulonodular lobes in each hemi-
sphere, the area ultimately responsible for balance. Proprioception stimuli arrive at the
anterior lobe, where posture can be maintained. The posterior lobe receives impulses
from the high centres of the cerebrum via the brainstem (Figure 14.10).
These cerebral connections allow the cerebellum to step in and control the ne coor-
dination of voluntary movement at a subconscious level, i.e. the cerebellum makes mus-
cle activity smooth, otherwise contractions would be jerky and erratic, especially for
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296 Neurological observations (IV)
From
putamen
LMN LMN
Muscle
Muscle
Vestibular
nuclei
Cerebellum
Red nucleus
Midbrain
Reticular
formation
Pons
Vestibular
nuclei
Medulla
Figure 14.10 T he pathways from the cerebellum that control balance by adjusting the body’s skel-
etal muscles (Figure 9.5, page 190). LMN: lower motor neuron.
fast movements. It also determines the extent and timing of muscle bre contractions. It
also increases muscle tone, providing a balance to the muscle tone function of the basal
ganglia, which decreases muscle tone (see page 294, Figure 14.7). It also learns and per-
fects the skills of co-ordinating synergy.
2
Cerebellar synergistic skills involve the ability to
coordinate muscle activity in relation to a moving object, using visual information from
the visual cortex of the cerebrum to plot the direction and speed of the moving object.
It works out the muscle response required to allow the chosen part, e.g. hand or foot, to
intercept with that object. It means predicting ahead, since it takes time to move a limb to
a new position, during which the object itself has moved. Children are born without these
skills, and both synergistic skills and balance are learnt and practised from an early age.
They are then pre-programmed, like many other motor skills, and function with very little
or no conscious thought. Since visual information is crucial for this function, the cerebel-
lum has some inuence and control over eyeball movements, vital in tracking moving
objects (see Chapter 13).
Reexes
Various reexes exist to provide stability during movement and fast responses to adverse
stimuli and are a safeguard against falling and injury (Pomfrett 2005). A reex consists of
a sensory input to the brain or cord, an integration or control centre and a motor response
output to the relevant muscle group (i.e. the components of a reex arc; Figure 14.11).
Painful sensory impulses pass into the posterior spinal cord and cross to the front on
the same side via a connector (or association) neurone to the cell body of an LMN. The
impulses from this LMN pass out of the cord to the muscle, which then contracts to pull
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Neurological observations (IV) 297
Posterior root
Pain
White of spinal nerve
stimuli
matter
Grey
matter
Anterior root
of spinal nerve
(motor)
Mixed
spinal
nerve
Muscle
Skin
(sensory)
PRG
LMN
Figure 14.11 The reex arc. A special sensory neuron takes painful impulses from the periphery to
the cord. Impulses pass to the brain, but at the same time interneurons cross the cord
from the posterior sensory to the anterior motor areas of the grey matter, and the lower
motor neuron conveys an impulse to the muscles to move the part from harm. LMR:
lower motor neuron; PRG: posterior root ganglion (see Chapter 12).
the limb away from the source of the pain. Deep tendon (or stretch extensor) reexes
include the patella reex, where the patella tendon is tapped below the patella bone
with a clinical hammer. The knee-jerk that follows is caused rst by stretching the sen-
sory muscle spindle within the thigh muscle with the hammer tap, thus sending impulses
into the cord. This then activates the LMN at the same level as the sensory input, and
motor impulses are sent back to the same muscle, making it contract slightly to correct
the original stretch. The exor (or withdrawal) response is created by the application of
painful stimuli to a limb, causing pain stimuli to pass into the cord. Again, an LMN res
in response to contract the exor muscles of that same limb while relaxing the extensor
muscles. At the same time, the impulse crosses the midline in the cord and causes the
opposite response in the other limb, which then extends (called the crossed extensor
response; Figure 14.12).
The muscles
The end organ of any motor system is the muscle, a specialist tissue with the function of
contraction and in the process produces heat (see Chapter 1). Muscles are of three types:
skeletal muscle, which is attached to the bones and serves to allow voluntary movement;
smooth muscle, which forms the walls of internal tubes, such as blood vessels and the
digestive tract and is involuntary and cardiac muscle in the heart wall, which contracts
involuntarily. Muscle is the only tissue in the body that can itself move; anything else that
moves, such as bones or blood, is moved by a muscle. Muscles pull but cannot push, but
smooth muscle constructed into a distinct ring around a tube wall can constrict to close
the tube lumen. This is called a sphincter.
3
In the limbs, skeletal muscles are set in opposing positions around joints, called
antagonistic pairs because these muscles have opposing functions: one muscle to
bend the joint (the exor) and one muscle to straighten the joint (the extensor; Figure
14.13).
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298 Neurological observations (IV)
Flexor
muscle
contracts
(withdrawal
from pain)
Painful
stimuli
LMN
LMN
LMN
LMN
Midline
Extensor
muscles
contract
(prevents
overbalance)
Figure 14.12 The crossed extensor reex. Painful stimuli affecting one side of the body cause exion
of the muscles on that side via the reex arc (Figure 14.11) in order to withdraw from
the pain. At the same time, impulses cross to the other side and stimulate extensor
muscles at several levels above and below the level affected to prevent overbalancing.
Humerus
Biceps
Radius
Tr iceps
Figure 14.13 Antagonistic muscle pairs. In this example, the exor is the biceps and the extensor is
the triceps muscles of the upper arm.
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Neurological observations (IV) 299
Once muscles have contracted they cannot return to a stretched state on their own.
Therefore, contracting the exor muscle stretches the extensor muscle, and vice versa.
Muscle contraction involves moving the insertion (the travelling and mostly the lower
end of the muscle) towards the origin (the xed and mostly the upper end of the muscle).
The nerve innervation of the various types of muscle are different: the skeletal muscle is
controlled by the pyramidal and extrapyramidal tract systems, the smooth muscle is con-
trolled by the autonomic nervous system (ANS) and the cardiac muscle is regulated by the
ANS. Between the nerve and the voluntary skeletal muscle is the neuromuscular junction,
a gap where a neurotransmitter called acetylcholine is active in passing the impulse from
the neurone to the muscle cells.
Movement observations
Disorders of movement can be classied according to the system that is causing the
problem, i.e. pyramidal or extrapyramidal tract disorders, basal ganglia or cerebellar
disorders, or diseases of the muscles themselves. Observations of movement are best
achieved in conscious patients, either by watching as patients attempt movement or by
requesting patients to undergo specic movements for the purpose of observation. Walk-
ing is a good opportunity to observe a patient’s ability to move, whereby different forms
of gait (i.e. the manner in which an individual walks) may be seen and balance can be
assessed. Loss of consciousness removes all such purposeful
4
movements and would
probably mean that any movements observed are likely to be spontaneous and probably
reex-type activities.
When assessing movement, the basic questions to establish are:
1 Can the patient walk properly, or are there noticeable difculties with mobility (e.g.
dragging one foot or being unable to balance)?
2 Can the patient talk properly, or are there noticeable problems with speech (e.g. slur-
ring of words)? Remember, not all speech problems are due to abnormal muscle activ-
ity, but there is a major motor component to speech.
3 Does the patient show any abnormal (non-purposeful) movements (see footnote 4),
such as shaking or inability to sit still?
Normal movements, i.e. the expected range and types of movement, are well understood.
This expectation makes abnormal movements quite obvious as patients make efforts to
get around and communicate.
Movement problems could be classied into losses and excesses. Losses (normal move-
ments that have been lost) include:
• hypokinesia, a general reduction in the level of movement (kinetics = movement,
hypo = lower than normal level)
• akinesia, the inability to initiate a movement, for example being unable to start to walk.
The letter ‘a’ before a word means without, i.e. akinesia literally means without move-
ment (due to being unable to start that movement)
• paralysis, a total loss of movement
• paresis, a weakness of muscle movement, a condition similar to – but less severe
than– paralysis.
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