Pathology of nervous system pathophysiology of nervous system and its functions

1. Associate Professor of Pathophysiology Department
Spirina Maria Aleksandrovna
mas.dokuments@yandex.ru

2.  The nervous system doesn't have the
reserves of oxygen and glucose
 60% of all glucose consumed in an
organism it is utilized by the nervous
system
 20% of all consumed oxygen fall to the
share of a brain
 15% of all blood expelled by heart come
to a brain

3.  The younger cells are most
sensitive to a hypoxia and to the
starvation
 The mental disturbance is revealed
already when PaO2 in arterial
blood decreases to 40 — 50 mm
hg. When PaO2 falls lower than 30
mm hg, through 20 seconds there
is a loss of consciousness, and still
through 20 seconds the electric
activity of a brain disappears.

4.  The cerebral blood flow is normal of 50 — 60
ml/min on 100 g of weight irrespective of
fluctuations of the average arterial tension
ranging from 45 to 170 mm hg.
 The global changes of a cerebral blood flow
arise or at strong falling of the arterial tension
(lower than 45 mm hg), or at the cerebral
edema.
 The brain tissues keep the viability at the
depression of a blood flow to 1/3 from normal
(to 15 — 20 ml/min. on 100 g of weight) within
30 — 60 min and only after this the changes in
a brain become irreversible.

5.  A pathological process in a
nervous system leading to
disorder of its activity, and also an
organism in general including
behavior and mentality, begins
with the damage of histological
elements of a nervous system,
first of all the neurones
(membranes, receptors, ion
channels, secondary
intermediaries, the genetic
device).

6.  the ability of neurones to
reorganize the synoptic contacts
to cells targets;
 the ability of a nervous system
to training and to the formation
of new skills.

8.  Internal causes
 Exogenous factors
 The Risk factors of damage of a nervous
system (condition):
the intensity, the duration, the frequency of influence
of this factor;
the condition of a nervous system at the time of
action of the pathogenic agent
 a condition of a hematoencephalic barrier

9. THE EXTERNAL CAUSES
The examples of pathogenic agents:
* The
mechanical
injury
* the ionizing
radiation
* A hypoxia
* The ethanol
* The organophosphoric
compound
* An abused drug
* The
neurotropic agents
(a strychnin, a curare)
* the microbes
(neurophilic exo-
and endotoxins of
microbes, for example
diphtheritic,
tetanic,
botulinic)
* A word
The daunt images
(“wraith”),
feelings
* The stressful
situations
chemical biological psychogenic
physical
The reasons of the nervous
system disturbances (1)

10. the biologically active
substance imbalance
and their effects
(neurotransmitters,
hormones, cytokines)
an
excessive
activation
of the free-
radical lipid
peroxidation
the disturbances
of vital activities and
structures of
tissues, organs and its
systems, bringing
to disorder:
the
disturbance
of the
thermal
homeostasis
in
organism
THE INTERNAL CAUSES
the circulation
of
blood and of
neurolymph in
brain and
spinal cord
the balance of
ions
and liquids
inside and out of
neuron
the
metabolism
in the
neuron
the structure and
the rheology of
blood and of
neurolymph
The reasons of the nervous
system disturbances (2)

11. THE CONDITIONS DEFINING the PATOGENICITY OF NEUROTROPIC
FACTORS
the force, the
duration,
the frequency,
the frequency of the
influences
the state of a
hematoencephalic
barrier
the state of a
nervous system
at the moment
of a factor action

12. The results of influences of
causal factors
The
functional
disturbances
of a nervous
system
The organic
disturbances
of a nervous
system

13. the autolysis of
the
neurone
components
nonspecific
THE MAIN MECHANISMS OF NEURON DAMAGE
(1)
the
membranes
damage
the disorder
of a protein
biosynthesis
the
imbalance of
ions and of
liquids
the
neurone
apoptosis
the disturbance
of the
power
providing

14. specific
THE MAIN MECHANISMS OF NEURON DAMAGE
(2)
the
transport of
mediator
disturbance
on the axis
cylinder
the
inactivations
disorder
and the
mediator
excisions
from a
synapse
the
disturbance
of mediator
allocations
in the
synaptic cleft
a mediator
interactions
disturbances
with a receptor
the
biosynthesis
of
neuro
mediator
disorder

15.  THE AFFERENT DISTURBANCES are the disorders
of a perception of various influences and a signalling
transduction from afferent structures to the nervous centers.
 THE CENTRAL DISTURBANCES are the disorders of
the analysis processes of the afferent signals, of the synthesis
and of the generation of an efferent signal by the nervous
centers.
 THE EFFERENT DISTURBANCES are the disorders of a
signalling transduction from the center and their perception by
the executive structures.

16.  The pathological process in a nervous system
begins with its damage (it is caused by the action of
factors of various nature).
 The damages are expressed in various destructive
and desintegrative phenomena, in disturbances of
chemical processes.
 These phenomena ⇒ condition and cause of
pathological process. Development is carried out by
the endogenic mechanisms arising again after and
owing to damage.
 The emergence of endogenic mechanisms
represents a stage of an endogenization of
pathological process without which process can't
develop!

17.  The role of a hematoencephalic barrier.
 Besides damaging, there are also sanogenetic
mechanisms preventing the emergence of
pathological changes in nervous system or
stopping these changes.
 The anti-system selectively prevents the
development of the corresponding pathological
system or suppresses its activity (an example: the
antinociceptive system emitting the β-endorphines
and enkephalins causing an analgesia).
 The genetically caused or acquired failure of anti-
system is the contributing factor and a condition of
development of pathological process.

18.  After each pathological process in the nervous system
there are structurally functional changes which can
remain in the form of the traces hidden in usual
conditions
 They aren't shown → 1) because of their weakening, 2)
because of the mechanisms of a compensation and a
tonic brake control from various structures of a nervous
system and, in particular, from anti-systems.
 At action of the new pathogenic agents activating the
hidden changes and breaking the control mechanisms,
the specified changes can functionally be shown → the
emergence of these or those symptoms. Such reactions
call afterimpression.

19.  The damage of nervous system formations ⇒ the disturbance
or a loss of their function.
 If the defect is shown clinically: it means that the pathological
changes became appreciable that the mechanisms of
compensatory defect lap are already insufficient ⇒! the pathological
process at this stage reached already an appreciable development.
 Around a damage zone in spinal or in a brain there is an inhibition
zone. It has a protective value, but on the other hand ⇒ it enlarges
and increases the functional defect.
 ! The restoration of function happens not due to neogenesis of
neurons, and due to normalization of the damaged cells and
decrease of inhibition of other neurons.
 The weakening and the loss of function can be bound only to deep
inhibition of the nervous education performing function (hysterical
paralyzes, the inspired loop functions).

20.  The neurones are under the constant tonic brake
control which doesn't allow to react to the
numerous casual impulses arriving from various
sources.
 The deficiency of inhibition can be primary owing to the
direct damage of brake mechanisms (a tetanin,
Strychninum) or secondary ⇒ the excessive activity of
neurons caused by the depolarizing agents and other
factors overcomes the inhibitory control.
 The mechanisms of brake control are sensitive to
various pathogenic influences and the adverse
conditions ⇒ Therefore the deficiency of inhibition
and a disinhibition of neurons take place practically
at all forms of pathology of a nervous system.

21.  It represents a complex of the changes arising in postsynaptic
neurons, organs and tissues in connection with the termination of
nervous influences on these structures.
 In a muscle it is shown by a disappearance of the end plate on muscle
fiber where there is a cholinergic device, and the emergence of the
acetylcholine receptors throughout a muscle fiber ► ⇑ a sensitivity of a
fiber to Acetylcholinum is observed. The result → the fibrillary
contractions of a denervated muscle.
 In a denervated muscle there is the range of enzymes of fetal type ► the
return of muscular tissue to fetal stages of development the result of a
loop of the controlling, trophic nerve influences → there is a
disinhibition of the genetic device of muscle fibers.
 The common pattern of a syndrome → ⇑ the increase of the sensitivities of
denervated structures not only to mediators, but also to other biologically
active substances and pharmacological agents.
 It can arise not only after a nerve break, but also at many forms of
pathology, under the influence of pharmacological agents, under the
blockade of neuroceptors.

22.  The impulsation coming to a neurone from any source is
an afferent impulsation for this neurone. The cessation
of this afferentation ⇒ a neuron deafferentation.
 There is no a full deafferentation of a neuron, because
the neurons possess a huge number of entrances of
impulsation from various sources.
 At a partial deafferentation there is a rising of
excitability of a neuron and a disturbance of the
locks. The partial deafferentation of neurons can take
place at various diseases of the nervous system.

23.  The neuron and the its structure form a regional trophic contour in
which there is a constant mutual exchange of the trophic factors
that are called trofogenes or trofins
 The dystrophic disturbances (ulcers) are a consequence of
deficiency in denervated tissues of the trophic factors controlling
the genetic device. There are changes of activity of a genome of
denervated structures ⇒ synthesis of proteins is broken and the
blasted intracellular structures aren't filled, the new proteins appear.
 An important role is played by a pathogenic trophic factor
(pathotrofogen) arising in patholologically changed cells and the
inducing pathological states (degenerin, a β-amyloid)

24. The generator represents the unit of the hyperactive
neurons producing an intensive, uncontrollable stream
of impulses.
It is a typical pathological process in the nervous
system.
The initial mechanisms of the emergence are

• stabile, an appreciable depolarization of neurons;
• disturbance of the neuron inhibition;
• partial deafferentation of neurons;
• trophic disorders;
• alteration of neurons and change of their medium and environment

25.  The obligate condition of formation and activity
- a failure of locks in populations of its neurons.
 The generator can develop self-sustaining and
even the increasing activity, without needing in
additional stimulation from the periphery or from
other sources.
 The meaning of the generators of the
patholologically intense exaltation - the
emergence of a neuropathological syndrome
 The generator can arise practically in all
departments of the nervous system
 The activation of the generator provokes attacks at
neuropathological syndromes.

26. Afferent impulse before coming to the highest departments of a
nervous system passes the intermediate centers (for example,
being in a spinal cord)
Through these intermediate centers the signal can be carried out
without change (simple relay transfer), but in some cases the
signal in the intermediate centers can be strengthened or
weakened.
The intensifying is carried out at the expense of the neurons, capable
to generate a volley of impulses in response to the arrived single
incentive, and due to existence of direct and return (exponential)
connections of neurones. The signal becomes weaker because of
the brake signals.
The force and the duration of exaltation of the intermediate center at
the same time increases.

27.  At a dominant the center of exaltation involves to
itself the exaltation from different departments of
the nervous system, but sends this exaltation on
some one way to a concrete effector.
 At the phenomenon of a station of universal
departure phenomenon the station is excited from
one afferent source, but sends exaltation to
different departments.

28. - The pathological reflexes are called the
reflex reactions which limit organism
devices, break its equilibration in the
environment.
- - Unconditional
- - Acquired

29.  deep oppression of the
brain functions
 loss of consciousness
 absence of reflexes
 disorders of the vital
functions

30.  Progressing dysfunction of central neurons
which govern body organs and systems
 Minimal excitation of neurons, which is
necessary for breathing, blood circulation and
other body functions

31.  1. Initial injury of the CNS (stroke, trauma).
 2. Endocrine diseases (diabetic, hypocorticoid, hypopituitary,
hypothyreoid, thyreotoxic, hypoglycemic).
 3. Intoxications , caused by organ failure (kidney, liver, pancreas)
and exogenous intoxications (alcohol, drugs, poisons).
 4. Different types of hypoxia
 5. Water and electrolytes imbalance

32. 1.Disorder of cellular breath and an exchange
of energy in the brain.
 Hypoxia
 Anemia
 Disorders of brain blood circulation
 Blockade of respiratory enzymes by
cytotoxic poisons, acidosis (in diabetic and
uraemic cоma)
 Deficiency of power substances or blockade
of their recycling (starvation, hypoglycemic
coma).

33. 2.Disorder of synaptic transmission in the central nervous
system. It may be connected with:
 a) disorder of synthesis, transport, deposition and
secretion of neuromediators;
 b) replacement of neuromediators by pseudomediators;
 c) excessive activation of inhibition postsynaptic
receptors;
 d) blockade stimulating postsynaptic receptors. This
mechanism has the great value in development of
hepatic, uremic and toxic comas.

34. 3.Disorder of electrolyte balance
 Changes in cellular membrane potentials
 Disturbances of neuron membranes
polarization
 Infringement of osmotic pressure.

35. Swelling and edema of brain
 Increase of intracranial pressure
 Disturbances of hemodynamic and liquor
dynamic
 Severe hypoxia

37. the disturbance
of the
movement
coordinations
– an ataxy
the depression
of a motive
activities and forces
muscular
constrictions at
the movement –
a hypodynamia
The typical forms OF NEUROGENIC CONTROL DISORDERS OF
MOVEMENTS
the restriction
of
movements
volume
and rates –
a hypokinesia
a redundancy of
the automatic
movements
– a hyperkinesia

38. The types of the hypokinesias
by prevalence
by expression by the casualty
nervous
structures
by changes in
the myogenic
tonus
a paresis central
spastic
A monoplegia
a paralysis A paraplegia peripherical
hyposthenic
A triplegia extrapyramidal
rigid
A tetraplegia
neuromuscular
A hemiplegia

39. THE SIGNS OF THE CENTRAL PARALYSIS
the
pathological
segmentary
reflexes
A clonus
A hyperreflexia A synkinesis
a muscular
hypertonia of
spastic
type
* consensual
muscular
reductions
* the series
of fast
rhythmical
reductions of
muscles

40. a degeneration of the
muscular
fibers
a redundancy of the
passive movements
in paralyzed
extremities
THE SIGNS OF THE peripherical PARALYSIS
A muscular
hypotonia
A decrease of
the muscular
irritability
A hypo- or
a muscle
atrophy
A hypo- or a
areflexia

41. THE SIGNS OF THE EXTRAPYRAMIDAL PARALYSIS
the muscular
hypertonia of a
plastic type
A muscle
tension A postural reflex
A
catalepsy

42. A masklike face
The parkinsonism
(a damage of the extrapyramidal system)
Tremor of
hands

43. THE ETIOLOGICAL FACTORS
the inhibition of
Acetylcholinum release in a
synapse,
its increased destruction by
cholinesterases
the hypoconcaveation
of the
holinoretseptor
myocytes
the decrease of
holinoretseptor number
on myocytes
(their blockade by the
antibodies)
the damageof the
holinoretseptors by
antibodies
the damage of
myocytes by
antibodies and by
the cytotoxic cells
THE DEVELOPMENT MECHANISMS OF THE
NEUROMUSCULAR PARALYSES (MYASTHENIAS)

44. By the damaged
areas of the nervous
system
By the prevalence
THE TYPES OF THE HYPERKINESIAS
* The
convulsions
* A chorea
*a tremor
*a palmus
* An athetosis
* A dystonic
torticollis
By the predominance of
“fast” or
“slow” movement s
stem
“fast” local
“slow”
cortical subcortical gеneral

45.  The convulsions are the sudden constructions of
muscles of various intensity, duration and
prevalence.
 Clonic. The short-term and irregular reductions of
separate groups of muscles, through small periods.
The widespread expressed clonic fits designate as
the fits.
 Tonic. The long muscular contractions, with
"hardening" of a trunk or extremities in various
compelled provisions.
 Admixed.

46. The chorea is the chaotic, fast, spasmodic,
violent reductions of various groups of
muscles. It is observed at a long ischemia of a
brain, at an atherosclerotic lesion, at a
rheumatic encephalitis, at the craniocerebral
injuries.

47.  The tremor is a hyperkinesia of trembling type. It is
characterized by consensual, stereotypic rhythmic
oscillating motions of a body or its parts as a result of
the repeating reductions and relaxations of muscles.
 It arises mainly at a brainstem lesion. It is observed
at organic lesions of a brain (multiple sclerosis,
Wilson-Konovalov's disease, an encephalitis, a blood
supply disorder), at the exogenous intoxication of an
organism (alcohol, Hydrargyrum, Morphinum).

48. The tic is the fast consensual stereotypic
reductions of a muscle or groups of muscles
causing the violent movements (for example, a
nictitation, a partially closed eyes, a
gesticulation).
It is observed generally at a lesion of extrapyramidal
system as a result of an encephalitis,
intoxications, including the medecines (for
example, at the use of psychopharmacological
agents), and also at some alienations.

49.  The athetosis is the consensual stereotypic,
slow worm-shaped movements resulting from
simultaneous long activation of muscles of
agonists and antagonists. Most often distal
departments of extremities are damaged.
 The dystonic torticollis is a deformation of a
neck and the wrong position of the head (an
inclination in one way) as a result of a long
spastic stricture of muscles of a neck.

50.  The ataxy is the locomotar disorders which
are characterized by the disturbance of a
spatial coordination of any movements. At
the same time the force of muscles is almost
not changed.
 The following organs take part in
coordination of movements: a spinal cord, a
mesencephalon, a thalamus, a cerebellum,
the frontal departments of a cerebral cortex,
a labyrinth.

51. THE TYPES OF ATAXY
(BY THE DEPENDENCE OF THE DAMAGED AREA)
The damaged area
* the back columns
of spinal cord
* the back roots
of spinal cord
* a visual hillock
* the peripheric
nerves
* a cerebellum
* the ways of a
cerebellum
* cortex of frontal
and/or temporal
occipital
areas
* a brainstem
* the area IV of a
brain ventricle
sensitive
(dorsal)
vestibular
(labyrinthine)
cortical
cerebellar

52.  A static form is a lack of coordination and
equilibriums in a standing and sitting
positions.
 A dynamic form is a disturbance of
performance of various movements by
extremities, especially by arms.
 A staticolocomotory form is a disorder of
coordination at standing and walking.

53. THE TYPICAL FORMS OF THE DISORDERS OF SENSATION
The damage of a
sensation type
the disturbance of the
adequacy
feelings
caused by it
stimulus
the disturbance of
intensity stimulus
perceptions
contact
distant
A thermalgia
A hypesthesia
A polyesthesia
An anaesthesis
exteroceptor A hyperesthesia An allodynia
interoceptor
A synesthesia
A hyperpathia
A paresthesia

54. The general mechanisms of the cacesthesia
“receptor”
the change of the
sensitivities
receptors threshold
“central”
the inhibition
or the blockade
of the
impulse
exaltations
“conductive”
decreased
increased
the change of the
sensitivities
neurones threshold
the change of
the receptors
numbers
the hypo -
hypersensitization of
the
receptors
the disturbance of
the
formations
feelings

55. The types of the hypesthesia and the anaesthesis
on the level of a sensory
system lesion
conductive
receptor
the "area" of a sensory
system lesion
central
fractional
total
osmetic
tactile
otopharyngeal
algesic
astereognosis
topoanaesthesis
other

56.  The pain is the special type of sensitivity
which is formed under the influence of a
pathogenic stimulus, characterized by the
unpleasant feelings, and also essential
changes in an organism up to serious
violations of its vital activity and even death.
 The pain can have alarm and pathogenic
value.

58. The value of the pain
alarm pathogenic
the reason and/or
pathogenesis
component of a
pathological
process
a mobilization
of the
organism
protective
reaction
a restriction
of the
organism
functions

59. The reasons of the pain
Physical (the
mechanical
trauma, the
raised or the
lowered
temperature, a
high dose of UF,
an electric
current, a prelum
of the edema).
Chemical (hit on
a skin or
mucosas of
strong acids,
alkalis, oxidizers;
the accumulation
in a tissue of
salts of a calcium
or potassium).
Biological (a high
concentration of
kinin,
Histaminum,
serotonin).

60. The types of the pain
Epicritical ("fast",
"first",
"precautionary")
pain results from the
influence of stimuli
of small and
average force.
Protopathic ("slow",
"burdensome",
"ancient") pain
arises under the
influence of strong,
"destructive", "large-
scale" stimuli.

61. the property of pain epicritical protopathic
the pain source skin, mucous the internals
a latent time short long
a duration after
elimination
It quickly stops It is observed very long
a threshold of sensitivity low high
a localization exact diffuse

62. The nociceptive system
The perceiving device:
- Nociceptors - the free
nervous terminations
which are activated only
at action of the
nociceptive agents
- Superstrong influence
on mechano-, chemo -
thermoreceptors can
also lead to formation of
feeling of pain
The carrying-out ways:
- Afferent conductors of
pain get into a spinal
cord through back roots
and contact to
intercalary neurones of
back horns.
- In a spinal cord the
convergence of
exaltation for different
types of painful
sensitivity ("false" pain)
is possible
Central nervous structures:
- Epicritical pain - result of
ascension of a painful
impulsation on a
thalamocortical way to
neurones of a
somatosensory zone of a
big brain cortex. The
subjective feeling of pain is
formed in a cortex
- Protopathic pain - result of
neurones of a forward
thalamus and subthalamic
structures

63.  The integrated feeling of pain at the person
is formed with simultaneous participation of
the cortical and subcortical structures
perceiving an impulsation about protopathic
and epicritical pain, and also about other
types of influences. In a cerebral cortex
there are a selection and integration of
information on painful influence,
transformation of feeling of pain into
suffering, formation of the purposeful,
realized "painful behavior".

64. The antinociceptive system
The neurogenic
mechanisms: the
descending ways from
neurones of gray substance
around ventricles of a brain,
a tire of the bridge, an
amygdaloid nucleus, a
hippocampus, separate
kernels of a cerebellum, a
reticular formation quashing
feeling of pain
The humoral mechanisms:
are presented by opioidergic,
serotoninergic,
noradrenalinergic systems of
a brain.

65. The vegetative (autonomous) nervous system
regulates the vital functions:
 respiration,
 blood circulation,
 digestion,
 metabolism,
 body temperature,
 reproduction.

67.  the disturbance of mechanisms of a
regulation of arterial pressure;
 the dysfunctions of external respiration;
 the disorders of a diaphoresis (dyshydrosis);
 the disturbance of the salivations;
 the disorders of functions of a bladder and
intestine;
 the disturbance of pupillary reflexes.

68.  The neurosis is a reaction of the person to a
difficult situation which is often not solvable.
 Mainly, the developing of neurosises start by
a neurotic conflict, i.e. such relation of the
person to a concrete situation which makes
impossible and "excessive" its rational
decision.

69. biological
• A genetic predisposition.
• a sex (the neurosis arises
less often at men).
• the age (the neurosis
develops more often in the
pubertatny and climacteric
periods).
• the constitutional features
of the person (the
asthenics are more
damaged of neurosises).
• The postponed and current
diseases reducing the
resistance of an organism.
social
• .The features of
professional activity (the
information overloads, the
monotony of labor
operations).
• the education level
• an unsuccessful marital
status.
• the unsatisfactory living
conditions.
• the features of the sex
education, etc.
• inconvenient workplace or
transport.
psychogenic
• the personal features (an
individual way of thinking, of
the perception, of the
behavior and response to
influences at this person).
• Mental injuries in the
childhood.
• The psychoinjuring situations
(a serious illness or loss of
relatives, the office or
"academic" difficulties).
• the formation of neurosis

70. The compulsion
neurosis The neurasthenia
The hysteric
neurosis
The CAUSES of the
EMERGENCE OF NEUROTIC STATES
AND SOME OF THEIR IMPLICATIONS
THE DISSOCIATION BETWEEN:
• needs of the person
and
• impossibility of
their realization
THE DISSOCIATION BETWEEN:
• the overestimated demands
of person to people around
and
• the impossibility
to realize them
THE DISSOCIATION BETWEEN:
• the overestimated demands
to person and
• the impossibility
to realize them
The signs
* the agoraphobia
*the social phobias
*The obessive and compulsive
disorders
* the simple phobias
* Inadequate (affective)
behavior
* The expressed vegetative
disorders
* The disturbances of movements
* the sensory disorders
* the sex deviations
* The vegetative disorders
* The increased excitability,
fatigability, "emaciation"
* The excessive irritability, fierines
* the performance decrement
* the instability of mood
* the disorders of a dream

71.  The reason: a dissociation ("conflict")
between desires, aspirations, needs of the
person and impossibility of their realization
for moral or other reasons.
 At the same time in a cerebral cortex the
pathological center of exaltation is formed.
Usually it occurs after one of episodes when the
person forgot to make something important (to
switch off gas, to close a door, to feed the child,
etc.) or transferred a condition of a pavor (height,
a stopping of the elevator, vulnerability).

72.  All kinds of obsessional states are
characterized by the repeating sensation of
fear, phobias of something and/or someone:
certain objects, activity, situations. The
beginning of neurosis of obsessional states
is formed on the mechanism of a conditioned
reflex. After a condition of emergence the
phobias extend.

73.  The types:
- Social phobias are the repeating absurd phobia, a pavor to fall into a
difficult or humiliating state in society: during the public
performance, reading a lecture, at examination, on a visit. Quite
often it really leads to failure and fixes a phobia.
- Obsessive and compulsive disorders are the obsessional, repeating,
"climbing" in the head ideas, thoughts, "orders" to make this or that
action. The person resists it, realizing and being afraid of
undesirability, absurdity and senselessness of such action (for
example, murders of a favourite being, the relative; the constant
washing of arms because of a pavor to catch or be soiled;the infinite
check of yourself—the closed door, the switched off gas, etc.).
- Simple phobias are the constant unmotivated pavors and/or
aspiration to avoid situations which can realize these fears (a
claustrophobia, a cancerophobia).

74.  The group of disorders is characterized by
imitation, but not simulation, by the patients of
illnesses and by rich somatoform disturbances.
The last is shown by excessive attention to the
health, unreasonable alarm for it, conviction
available of illness which actually is absent. At
hysteria, as a rule, there is "desire of illness" and
high suggestibility. A polymorphism of hysterical
disorders, their deliberate, demonstrative and
exaggerated character is explained by it.

75.  the inadequate behavior. Affectivity,
impressionability, suggestibility and
autosuggestibility, instability of mood, forgetfulness.
Hysterical emotional and affective disorders are
followed by theatricality and affectedness of
experiences, their confinedness to certain situations.
People with hysterical neurosis try to make an
impression of very busy, significant, influential
persons, being the center of events. Actually they
are, as a rule, persons fine, perfunctory, fussy,
dependent on other people.

76.  the vegetative disorders (for example, hypo - or
hypertensive reactions, a dyspnea, inflows of "a
hot blood", tachycardia, an arrhythmia, a
sweating, the dyspeptic disorders).
 the motive disorders. Convulsive attacks are
possible (without a loss of consciousness and
bruises!), the transient paresis and paralyzes;
the short-term aphonia because of paralysis of
vocal chords is possible.

77.  the sensory disturbances. Hysterical
neurosis quite often is followed by a transient
blindness, deafness, a loss of an olfaction, of
taste, by the paresthesias.
 the sex deviations (for example, impotency,
depression of a libido).

78.  the reason: a dissociation ("conflict")
between demands to (as a rule,
overestimated) and impossibility to realize
them. It causes an overstrain and failure of
process of cortical exaltation.

79.  the vegetative disorders (the disturbances of a heart
rhythm, the hypo-or hypertensive reactions, the
gastrointestinal disorders, the increased sweating).
 The increased excitability, fatigability and emaciation of a
nervous system.
 Excessive irritability, fieriness, impatience.
 the disorders of attention, disturbance of its concentration.
 The reduced working capacity, slackness.
 the instability of mood, it is frequent a depression.
 the disorders of a dream (a backfilling disturbance, an
uneasy dream, the unpleasant dreamings).

80. Thank you for your
attention!
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