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_3050_Библиотеки_им_академика_М_И_Перельмана
.pdf
300 Neurological observations (IV)
Excesses movements. i.e. unwanted movements that occur that the patient cannot control
include:
• dyskinesia, an obvious abnormal movement
• hyperkinesia, an increase in involuntary movements, such as tremor, which is an
uncontrolled shaking of limbs (hyper = greater than normal)
• akathisia, a motor restlessness that prevents the individual from sitting down.
Movement losses
Paralysis and weakness
A total loss of the ability to move is paralysis, a major neurological decit that may be
local (e.g. in one limb) or involve wider aspects of the nervous system. Hemiplegia, a
paralysis of either the left or right side of the body, may affect those suffering from a
cerebrovascular accident (CVA – or stroke) to various degrees. CVAs are disruptions
to the blood supply of the brain, resulting in brain damage. This very often involves the
motor cortex and the major pathways from this area, the pyramidal tracts. Since these
tracts mostly cross in the medulla (Figure 14.1), a left hemiplegia indicates a stroke on
the right side of the brain, and vice versa. The degree of movement loss depends on the
extent of the brain damage and its location within the brain. Small bleeds close to the
brain surface may only result in weakness on one side, called a hemiparesis, with good
prospects for some or total recovery. Larger or deeper bleeds may cause more profound
paralysis with some permanent decit. A CVA is an example of a UMN lesion leading to
spastic paralysis in the longer term, where spastic means the stiffening and contracture
of the muscles of the affected limbs if adequate preventative measures are not taken. The
arm is usually held in a bent (= exed) position and the spastic hemiparesis creates a
characteristic gait where the leg circles stify outwards then inwards with a pointed toe
while walking.
Unlike hemiplegia, paraplegia results in the loss of function of the lower limbs, and
mobility often requires a wheelchair. Paraplegia is largely associated with spinal injuries
where the cord is damaged, severing the pyramidal motor tracts at a point in the tho-
racic or lumbar regions. Such trauma cuts off any opportunity for the brain to control the
muscles below the level of the injury. Of course, it could also affect the sensory neurons
as well, causing sensation losses in the lower limbs. A similar injury higher up the spine
in the cervical (neck) region may include a loss of movement below this level (i.e. a
tetraplegia, involving all four limbs and the trunk). Another cause of lower limb paralysis
is poliomyelitis, an infectious disease that damages the cell body of the LMNs or their
axons passing from the cord. LMN lesions result in a accid paralysis, where muscles of
the paralysed limbs become loose and oppy (loss of muscle tone) with complete loss
of reexes, and foot drop, a failure of the muscles that retain the foot at the normal right
angle to the leg.
The loss of the ability to perform purposeful movements is apraxia (a = without, praxia=
performing movements), i.e. the movements that occur are meaningless. The problem is
not caused by simple paralysis or weakness, nor is it due to a lack of comprehension or
motivation. It may be the result of a lesion in the parietal association cortex (see page 221)
along with disturbance to sensory interpretation and integration. Different forms of
apraxia may occur, and this depends on which side of the brain is affected. Dyspraxia
https://t.me/medicina_free
Neurological observations (IV) 301
(dys = difculty, praxia = performing movements) is the difculty in carrying out skilled
movements with no evidence of disorder of the primary motor pathways. This is not the
same as paralysis, which usually does involve the primary motor pathways. Apraxia and
dyspraxia are functional developmental disorders of differing severity; apraxia is a total
loss of purposeful movements and dyspraxia is a difculty in carrying out skilled purpose-
ful movements. Both disorders disturb the development of different systems, e.g. verbal
dyspraxia (speech difculty and delay), or motor dyspraxia (difculty with body move-
ment coordination, including balance and walking). A child with motor dyspraxia may be
called a clumsy child.
Another motor problem is multiple sclerosis (MS), an autoimmune disease of the neu-
ronal myelin sheath, which breaks down and is replaced by scar tissue (i.e. it is a demy-
elination disease). Autoimmune diseases occur when the body’s immune system identies
part of the body as foreign (or alien) tissue and begins to destroy it. The reason is not fully
known but viral infections of the affected tissues are suspected. MS can affect any neuron,
motor and sensory, and it causes a wide range of symptoms of varying degrees that can pass
from remissions (periods of no or few symptoms) to relapses (periods of worse symptoms).
Those signs affecting movement include spastic limb weakness with exaggerated reexes (a
UMN pyramidal sign) and an ataxia (i.e. loss of balance, a cerebellar sign; see page 296).
Motor neuron disease (MND) is another progressive degeneration of motor neurons,
this time the pyramidal (corticospinal) tract bres, some cranial nerve nuclei and some
LMNs within the cord. It causes severe movement losses involving motor control of mul-
tiple muscles, including the swallow reex, and death occurs within a few years. The
usual age of onset is 40–60 years. There are now around 25 gene mutations identied in
the causation of motor neuron disease. Some of these are inherited (i.e. run in families),
which is estimated between 7 to 10% of cases. The following is some information on the
main genes
5
involved (Corcia et al. 2008):
1 The gene superoxide dismutase-1 (SOD1, found 1993) on chromosome 21q. It codes
for the enzyme superoxide dismutase 1, which is a cellular defence against free radi-
cals which damage cells. Over 150 gene mutations are known in this gene, one of the
commonest being a codon change from alanine to valine.
2 The gene angiogenin (ANG, found 2006) is an autosomal dominant gene on chromo-
some 14q. It codes for a protein that is both an enzyme and a blood vessel growth fac-
tor (angiogenesis is the growth of new blood vessels). Patients with this gene mutation
have predominant bulbar symptoms.
3 The gene TAR DNA-binding protein (TARDBP) on chromosome 1p. It codes for the
protein TAR DNA-binding protein 43 (TDP-43). Normally, this protein has important
functions in gene transcription and translation.
4 The gene chromosome 9 open reading frame 72 (C9orf72, found 2011) on chromo-
some 9p. This is a DNA sequence repeat. The gene normally has up to 20 repeats,
while sufferers have hundreds of repeats. It affects about one-third of all familial MND
sufferers.
5 The gene fused in sarcoma (FUS, found 2009) on chromosome 16p. It codes for a
protein that has multiple functions within the nucleus of motor neurons, but mutations
cause this protein to accumulate outside the nucleus.
Research on MND is also focused on axonal transportation. This is the transportation of
substances, notably proteins, up and down the axon of neurons. This ow of proteins from
https://t.me/medicina_free
302 Neurological observations (IV)
neuronal cell body to the synapse and back is critical to synaptic and neuronal function.
Disruption of this process leads to synaptic malfunction and ultimately to motor neuron
losses.
Three different aspects characterise this disease:
1 progressive muscular atrophy (PMA)
2 progressive bulbar palsy (PBP)
3 amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease).
Most of the discovered genes are linked to the causation of ALS.
Patients with this disorder will rst develop one of these three aspects rst, either:
1 Muscular atrophy; i.e. loss of muscle bulk also called muscle wasting
2 Bulbar symptoms, i.e. paralysis of the mouth, throat or facial muscles, including dif-
culty in swallowing
3 Muscle weakness with twitching and some degree of paralysis.
These symptoms will remain dominant as other symptoms occur. Most patients will even-
tually show signs of all three to varying degrees. Those in whom PMA is dominant have
the least severe form and can have a survival rate of up to 15 years or more. PBP causes
deterioration of parts of the brainstem, and it has the worst symptoms and the shortest
life expectancy. It causes deterioration of swallowing, with choking on food and muscle
paralysis of the tongue and throat including speech loss. ALS is a progressive combination
of amyotrophy (i.e. muscle wasting caused by a loss of LMNs) and lateral sclerosis, a loss
of UMNs in the corticospinal tracts of the spinal cord. The main features are muscular
weakness and atrophy (= wasting of muscles), with fasciculation (= twitching of muscles)
in two or more limbs. The intellect and sensory systems are completely unaffected and
remain intact throughout.
Unfortunately, there is currently no treatment available for MND, but extensive research
is well underway and making progress towards a treatment.
Muscular diseases
Muscular diseases also cause weakness and paralysis. Myasthenia gravis is a disorder of
the neuromuscular junction. Acetylcholine (see page 299) cannot bind to the receptors
properly and muscle cells are unable to sustain repeated contraction during exercise so
that they fatigue quickly. The receptors are blocked by antibodies, plus there is a reduced
amount of acetylcholine available at the synapse. The thymus gland, part of the lym-
phatic and immune systems in the chest, may be the site of production of the antibodies
concerned, and removal of this gland, plus drugs to improve acetylcholine function, are
options for treatment.
The various muscular dystrophies form a group of disabling diseases involving the
muscle itself. Several of these disorders are genetically inherited, such as Duchenne mus-
cular dystrophy (DMD). This disease is the commonest in the group and affects mostly
boys because the gene involved (the DMD gene) is on the X chromosome.
6
Normally,
the gene codes for the protein dystrophin found in muscles. The role of dystrophin is
to strengthen and protect muscle proteins as they contract and relax. In DMD, muscles
become weakened and damaged due to the repeated muscle contraction, leading to
https://t.me/medicina_free
Neurological observations (IV) 303
deterioration in walking and other movement, with complete mobility loss by the time of
adolescence. It can affect cardiac muscle, and life expectancy may be short, i.e. death by
around 30 years.
Myopathies (myo = muscle, path = disease) is the term used to describe a failure of
muscle development with weakness, muscle pain and cramps early in life, again often
due to genetic inheritance. The weakness may be severe and cause major mobility dif-
culties that can be progressive throughout life.
Increased muscle tone (rigidity)
Disturbances to basal ganglia function, as in Parkinson disease, can cause an increase in
muscle tone, known as hypertonia; i.e. muscles become stiff and rigid and fail to allow
full body movement (Figure 14.14).
In Parkinson disease, the limbs are severely limited in function; the legs show a shuf-
ing gait and sufferers cannot lift their feet properly. The body takes on a forward stance
and often moves faster than their feet can. Patients may therefore lose their balance and
fall forwards. Carers observing these patients should be aware of the potential for injury.
Stooped
posture
Shuffling
gait
Masked
face
Forward
stance
Stiff arms
Hand
tremor
with pill
rolling
Figure 14.14 The signs of Parkinson Disease.
https://t.me/medicina_free
304 Neurological observations (IV)
The muscle tone increase is due to the failure of the basal ganglia’s role of inhibiting
excess muscle tone, causing stiffness in the muscles. James Parkinson, a Shoreditch apoth-
ecary surgeon, described the condition as paralysis agitans, i.e. agitated paralysis, which
neatly describes the two main features: body rigidity and limb tremor, especially the
hands along with ‘pill rolling’.
7
They suffer gradual loss of speech and the ability to write.
Parkinson’s disease is progressive due to the relentless destruction of the substantia nigra,
8
with a corresponding gradual loss of the neurotransmitter dopamine in the pathway from
the substantia nigra to the corpus striatum, the nigrostriatal pathway. The reason for the
loss of cells in the substantia nigra is unknown and cannot be prevented and will eventu-
ally lead to the patient’s death. It would appear that the symptoms do not occur until the
dopamine loss reaches 80%, indicating the asymptomatic (= without symptoms) onset of
this disease, which is very gradual over a number of years. On average, the age that symp
-
toms become obvious is about 60 years or more, but the process leading to those symp-
toms must have started considerably earlier in life. Treatment is aimed at the replacement
of the dopamine in this part of the brain, effectively reducing the symptoms – particularly
the rigidity – and therefore improving the quality of life.
Other forms of rigidity are decortication, an abnormal exion response and decerebra-
tion, an abnormal extensor response of the limbs (Figure 14.15). The symptoms of these
disorders and their causes are shown in Table 14.1. Decerebrate symptoms can be severe
enough to include stiff clenching of the jaw, neck extension and arching of the back.
Explanation of the terms in Table 14.1 are as follows:
• Adduction
9
is movement of a limb towards the midline of the body (i.e. held against
the side of the body).
• Internal rotation is a twisting of the limb inwards.
• Pronation is a palm downwards position of the forearm and hand (see Figure 14.15).
• Extension is straightening of a limb.
• Flexion (or hyperexion) is bending (or excessive bending) of joints.
• Plantar exion is a downward movement of the foot; the toes point away from the
body at an angle of as much as 45° from the normal right-angle position of the foot.
Ataxia
Ataxia is a difcult and abnormal gait, or walking, with specic forms of ataxia indicating
certain neuromuscular disorders (Bastian 1997). The gait of spastic hemiparesis seen in
CVA and the shufing gait of Parkinson disease have both been described (see pages 300
and 303). Cerebellar ataxia is caused by a disorder of the cerebellum or its tracts. It
produces an unsteady staggering gait with difculty on turning, and balance loss when
the feet come together, so the feet are usually held apart. This is often seen as a result of
alcohol intoxication. Sensory ataxia is an unsteady gait where sensory feedback from the
feet or legs to the cerebellum is lost. Again, the feet are held wide apart to help stabilise
balance. During walking, each leg is lifted high followed by the foot being slapped on
the oor. Since the patient is unable to feel the oor, it becomes necessary for the patient
to watch the ground to ensure his/her foot is safely in contact before putting any weight
on it. It is due to a destruction of the somatic sensory pathways of the spinal cord, as in
tabes dorsalis, a spinal cord complication of the infectious disease syphilis. Scissor gait
is caused by a bilateral spastic weakness of the leg muscles. The legs are moved slowly
forwards over short steps; the thighs tend to cross over each other in turn.
https://t.me/medicina_free
Rigidity Arms Legs Cause
Decortication Hyperexion of each Extension of legs with A high cerebral
of the joints with internal rotation and lesion interrupting
adduction of the limb plantar exion of foot the corticospinal
(pyramidal) tracts
Decerebration Elbow extension, Stiff extension of legs A hypothalamic or
wrist exion with with plantar exion of thalamic lesion
limb adduction and foot involving the brainstem
pronated forearms
Neurological observations (IV) 305
Decorticate Decerebrate
Figure 14.15 Decorticate and decerebr ate symptoms. In decorticate symptoms, the elbows, wrists
and ngers are exed with adduction of the arms, the legs are inwardly rotated, and
the feet are plantar exed. In decerebrate symptoms, the head is extended with the
jaws clenched shut, the arms are adducted with stify extended elbows, the forearms
are hyperpronated and the wrists and ngers are exed, the legs are stify extended,
and the feet are plantar exed.
Table 14.1 The symptoms and causes of decortication and decerebration
https://t.me/medicina_free
306 Neurological observations (IV)
Movement excesses
Tremor
The uncontrollable and involuntary shaking seen in the limbs in Parkinson disease comes
in two forms: a coarse tremor noticed in the whole limb and a ne tremor found in the
hands and ngers (Figure 14.14). This ne tremor has been called pill-rolling, since this is
the action taken during the manual production of pills before mechanisation and qual-
ity control. Parkinson’s tremor disappears as the limbs are put into conscious motion but
return at rest. Tremor is a very noticeable symptom and is very destructive of the patient’s
condence, motor activities and natural behaviour patterns.
Tremor may also be the result of multiple sclerosis, strokes, brain injury, various neuro-
degenerative disorders and even excess consumption of some drugs (e.g. amphetamines
and caffeine), alcohol abuse and withdrawal, hypoglycaemia (low blood glucose levels),
sleep deprivation, thyroid hormone excess, anxiety and stress. Some nutritional decien-
cies (e.g. magnesium and niacin) also show tremor as a symptom.
Athetosis, chorea and ballism
Huntington disease is a genetically inherited disorder caused by a gene mutation on the
fourth chromosome (Bentley 1999). It results in a progressive degeneration of several
areas of the brain, in particular the corpus striatum (composed of the caudate nucleus
and putamen) of the basal ganglia, with cell losses in the frontal and parietal lobes of the
cerebral cortex. Unwanted involuntary movements are a characteristic of this disease,
and these are athetosis (slow writhing movements of the limbs, face and tongue) and cho-
rea (fast twitching of whole limbs and body). If these two movements occur together, the
words are combined (i.e. choreoathetosis). The major distinctions between them are
thespeed (sudden chorea movements compared with the slow athetosis movements) and
the nature of the movement (in chorea, jerky and twitching movements; in athetosis,
writhing movements). Observers will note that the patient appears to be unable to sit
still. Chorea can sometimes occur in children (Sydenham chorea), often as a result of
rheumatic fever, caused mostly by an immune response to the bacterium Streptococcus.
The child or adolescent shows sudden, irregular and uncontrolled movements of no real
purpose, but unlike Huntington’s disease this is not a permanent problem (Gasser and
Kieburtz 2000).
Uncontrolled violent movements of a whole limb, involving inging the arms suddenly
in any direction, is called ballism. The appearance of this phenomenon may be sud-
den and frightening. Monoballism is the term used if a single limb only is involved, and
hemiballism indicates that both limbs on one side are affected. The violent nature of this
movement is due to the involvement of the subthalamic nucleus in the lesion.
The immobile patient
Immobility reduces independence to varying degrees. Observations of the immobile
patient are critical to understanding the patient’s needs, for identifying the early stages
of the complications of immobility and for maintaining the patient’s progress towards
mobility. In this observation checklist, the complications directly caused by immobility
are shown in italics.
https://t.me/medicina_free
Neurological observations (IV) 307
Observations checklist
1 Observation of the skin is vital for:
a Assessing for any dehydration (i.e. when the skin is dry and can be pulled into folds
that remain when released). Dehydration is a severe lack of uids in the tissues,
both the intracellular uids (intra = inside, cellular = the cells) and the extracellular
uids (extra = outside; also known as tissue uid; see Chapters 6 and 10)
b Preventing decubitus ulcers (= pressure sores), caused both by constricted blood
supply to the tissues when compressed by body weight and by friction eroding
the surface of the skin when the patient is moved around the bed. Assessment of
a patient’s risk of skin breakdown is often made using the Waterlow scale (Baxter
2008) or the Norton scale (Lewko et al. 2005; see Chapter 10)
c Assessing for poor personal hygiene and maintaining cleanliness.
2 Observing the mouth is vital for:
a Preventing dehydration, which could result in a dry mouth with poor saliva produc-
tion (see Chapter 6)
b Preventing infections, which could cause red, swollen gums and halitosis (foul-
smelling breath), pain and difculty with eating, and the risk of complications, such
as throat, chest, ear and brain infections.
3 Observing the urine is vital for:
a Assessing the output to maintain uid balance and reduce the risk of renal disorders
(see Chapter 8)
b Preventing urinary tract infections (see Chapter 8).
4 Observing the bowel function is vital for:
a Assessing the output to prevent constipation or diarrhoea (see Chapter 9).
5 Observing the level of consciousness is vital for:
a Prevention of confusion or coma (see Chapter 11).
6 Observing the respirations is vital for:
a Maintaining adequate ventilation and oxygenation (see Chapter 5)
b Preventing chest infections (see Chapter 5).
7 Observing body temperature is vital for:
a Assessing the patient’s ability to control body temperature (see Chapter 1)
b Preventing or detecting any underlying infections.
8 Observing the ability to communicate is vital for:
a Assessment of mental function, especially mood, which may be depressed
b Assessment of problems such as pain, and maintaining a pain-free state (see
Chapter12).
9 Observing the ability to eat and drink is vital for:
a Assessing the patient’s nutritional status (see Chapter 7)
b Preventing hunger, dehydration and malnutrition.
https://t.me/medicina_free
308 Neurological observations (IV)
Table 14.2 Red ag warnings of deteriorating mobility condition
O Red Flag = serious situation which needs urgent medical attention.
Flag warning Details
O Red Flag
Rapid onset of weakness or paralysis of one side of the bod
y (Chapter 11).
(After Hill-Smith and Johnson 2021, with permission)
10 Observing the sleep cycle pattern is vital for:
a Assessing that the patient has enough rest.
11 Observing the pattern of mobility possible in each limb and joint is vital for:
a Assessing what mobility the patient can achieve and maximising this to prevent
joint stiffness and muscle atrophy (muscle atrophy = wasting of the muscles, or loss
of muscle bulk; see page 302)
b Assessing what mobility assistance the patient will need in terms of professional
help (such as physiotherapy) and mobility aids (such as a wheelchair) to prevent
excessive periods of immobility.
Immobility disrupts all aspects of daily life, both physically and mentally. Given what is
known about the complications of immobility, maximum possible mobility should be
established and maintained. Immobility should not mean long periods conned to a bed
or chair.
Key points
The neurobiology of human movement
• Pre-programming of movement is the essence of the learning process and allows move-
ment to occur at a subconscious level.
• The motor cortex cells are arranged in a manner that reects the basic body plan.
• The pyramidal tracts descend from the motor cortex.
• The pyramidal system is two-neuronal, consisting of an upper motor neurone (UMN)
from brain to cord and a lower motor neurone (LMN) from cord to muscle.
• The extrapyramidal system controls voluntary movement at a subconscious level.
• The basal ganglia have a role in controlling slow, sustained movements and in main-
taining muscle tone.
• Muscle tone is a state of tension of the muscle essential for contraction.
• The cerebellum is important for balance, posture, smoothing out muscle movements
and synergistic skills.
• Reexes provide stability during movement and fast responses to adverse stimuli. A reex
arc has a sensory input to the cord, a control centre and a motor output to the muscle.
• Muscles are of three types: skeletal muscle attached to bones, allowing voluntary
movement, smooth muscle forming walls of internal tubes, allowing involuntary move-
ment and cardiac muscle in the heart wall.
• The various types of muscle have different nerve innervation: skeletal muscle is controlled
by the pyramidal and extrapyramidal systems, smooth muscle is controlled by the auto-
nomic nervous system and cardiac muscle is regulated by the autonomic nervous system.
https://t.me/medicina_free
Neurological observations (IV) 309
Disorders involving movement
• Paralysis is a loss of movement: hemiplegia is paralysis of either the left or right half of
the body, paraplegia is paralysis of the lower half of the body and tetraplegia is paraly-
sis of the body from the neck down.
• Cerebrovascular accident (CVA) or stroke is a bleed into the brain or an obstruction of
the blood supply to the brain.
• Poliomyelitis is an infectious disease that damages the cell body of the lower motor
neuron.
• Multiple sclerosis is an autoimmune disease of the myelin sheath, which breaks down
and is replaced by scar tissue.
• Myasthenia gravis is the inability of acetylcholine to bind at the neuromuscular junc-
tion, which causes the muscles to be unable to sustain repeated contraction.
• Muscular dystrophies are often genetically inherited. Duchenne’s muscular dystrophy
affects mostly boys. Fat accumulates in the main muscles during childhood, leading to
deterioration of walking with complete mobility loss by the time of adolescence.
• Parkinson disease is a degeneration of the basal ganglia, causing an increase in muscle
tone resulting in rigidity and tremor.
• Decortication is an abnormal exion response caused by a high cerebral lesion inter-
rupting the corticospinal (pyramidal) tracts. Decerebration is an abnormal extensor
response caused by a hypothalamic or thalamic lesion involving the brainstem.
• Ataxia is difcult or abnormal gait (method of walking).
• Motor neuron disease is a progressive degeneration of neurons of the pyramidal and
bulbar tracts.
• Huntington disease is a genetically inherited disorder resulting in a progressive degen-
eration of the corpus striatum with cell losses in the frontal and parietal lobes.
• Unwanted involuntary movements are called chorea (sudden and jerky movements)
and athetosis (slow writhing movements).
Notes
1 Movements with regards to talking involves learning to speak a language as well as control of the
lips, tongue, jaw and throat muscles.
2 Synergy is the combination of systems (e.g. multiple muscles) working together to achieve an out-
come that is greater than what is possible with only one of those systems working alone (e.g. one
muscle). On a broader scale, synergy is also the combination of different systems (e.g. muscular
coordination with the visual system) to achieve a goal that one system alone cannot achieve (see
vestibulo-ocular reex, Chapter 15).
3 A sphincter is a distinct muscular ring strategically located at sites along a tube to act like a
doorway (i.e. it opens or closes that tube). They are mainly smooth muscle but are differently ar-
ranged to the smooth muscle which is distributed throughout the tube wall and can act generally
to squeeze the tube contents forwards. Some external sphincters are skeletal muscle (notable the
external anal sphincter) and can be consciously controlled.
4 Purposeful movements are those that are deliberately and consciously carried out by the patient
to achieve a purpose. Non-purposeful movements are those that occur automatically without
conscious control and serve no purpose. Non-purposeful movements are often annoying to the
patient and indicate a potential problem.
5 It is important to remember that these genes are present in everyone, and only cause disease
when present as an abnormal mutation.
6 Females have two X chromosomes, so if one has the mutated gene then they most probably have
an alternative normal gene on the second X. Males only have one X chromosome, so if that X has
https://t.me/medicina_free
Соседние файлы в папке Библиотека им академика М.И. Перельмана