Wernicke manna pose is observed in patients who have undergone. Treatment with a position for central paresis (posture opposite to the Wernicke-Mann position). Extensive cerebrovascular accident: causes, symptoms, treatment and consequences

Decorative 10.08.2021

Decorative

Karl Wernicke (1848-1905)

Ludwig Mann (1866-1936)

Specific pathological changes in muscle tone in the affected limbs in the pathology of the pyramidal system. Acute unilateral lesion of the pyramidal tracts on the upper limb the muscles that raise the belt of the upper limb, the muscles of the shoulder that abduct and rotate outward, the extensors and arch supports of the forearm, the extensors of the hand and fingers, are more often affected; on the lower limb- muscle groups that abduct and adduct the thigh, flex the knee and foot. When the flaccid stage of hemiplegia is replaced by spastic, the antagonists of these muscle groups are especially hypertonic. Spasticity, if it is sufficiently pronounced, leads to the formation of contractures. As a result, the upper and lower limbs assume the following position: the belt of the upper limb is lowered, the shoulder is adducted and rotated inwards, the forearm is pronated and bent at the elbow joint, the hand and fingers are bent, the thigh is extended and adducted, the lower leg is unbent, the foot is in the pes equino-varus position, as a result of which the paretic limb becomes, as it were, longer than the healthy one.

when walking, do not touch the toe of the floor, the patient, not being able to raise the limb up, “mows” it, i.e., takes it to the side, describing a semicircle with the foot (“the hand asks, the leg mows”). The Wernicke-Mann position is more often observed in capsular hemiplegia (damage to the pyramidal tract in the region of the posterior leg of the internal capsule).

Wernicke-Mann position in a patient with left-sided hemiparesis (source: www.iqb.es/galeria/arpati10.htm)

Described by the German neurologist and psychiatrist Carl Wernicke (1848-1905) in 1889. ( Wernicke K. Zur Kenntnis der cerebralen Hemiplegie // Berliner clinic Wochenschrift, 1889. – bd.26. – S.969-970 ) and his student, the German neurologist and physiotherapist Ludwig Mann in 1896. ( Mann L. Klinische und anatomische Beiträge zur Lehre von der spinalen Hemiplegie // Deutsche Zeitschrift für Nervenheilkunde, Berlin, 1896. - Bd.10. – S.1-66).

Source: www.neurosar.ru

GAIT

Great Encyclopedia of Psychiatry. Zhmurov V.A.

Gait- posture and character of body movements while walking. Some types of gait have diagnostic value, their names indicate the nature of the disorder causing them or the psychological state of the individual:

atactic ("drunk" or stamping) gait;
hemiplegic or squinting gait (the injured leg is moved to the side and, without bending, makes a semicircle);
parkinsonian ("doll") gait - with small steps, with an unbending trunk and without synergistic hand movements;
cock's gait (steppage) with damage to the peroneal nerve (the leg rises high and then slaps on the floor;
frontal ("fox") gait with the setting of the feet in one line;
hysterical "flying feather" gait (or Todd's gait) - with large jumping steps and stops right in front of the obstacle;
senile gait - small shuffling steps with insufficiently coordinated hand movements;
sweeping gait with hysterical hemiplegia, when the paralyzed leg is dragged with a “broom”, and does not “rake”, as is the case with true hemiplegia;

dancing gait with choreiform hyperkinesis (legs are widely spaced, many unnecessary and uncoordinated movements are made, the patient is suddenly thrown from side to side);
duck gait, observed with myopathy and subluxations in the hip joints (rolling over from side to side due to hypotension of the muscles of the pelvic girdle). Gait changes strongly and in certain ways in depression, mania, catatonic substupor and agitation, in the neuroleptic syndrome, during an acute reaction to stress, and, it is possible, in many other disease states. Finally, important information for an observant person contains gait and about a person’s character, his lifestyle, profession, age, gender identity, and mood.
stealth gait (hands rest firmly in pockets during movement);
decisive gait (quick, with sweeping hand movements);
depressed gait (head down, legs dragging, hands in pockets);
impulsive gait (energetic with hands on hips, giving way to lethargy, "lethargy" - Churchill's gait);
the gait of the dictator (with his head raised up, stiff legs and emphasized energetic movements of his hands - Mussolini's gait);
thinker's gait (ritually unhurried, often with hands behind his back or with some familiar object in his hands - Helmholtz's gait).

Dictionary of psychiatric terms. V.M. Bleikher, I.V. Crook

Gait- a set of features of the posture and movements when walking. Some types of gait have diagnostic value, for example, atactic gait (see Ataxia); hemiplegic (see. Hemiplegia, Hemiparesis) gait (the paretic leg is retracted to the side and, without bending, produces a semicircle - hence: squinting, circulating gait). With parkinsonism, a puppet gait is observed - with small steps, without synergistic hand movements, with a frozen and unbent torso. With damage to the frontal lobes of the brain - fox P. (setting the feet in one line). In hysteria, there is a gait of a flying feather - large steps, jumps, the patient stops only when he stumbles upon an obstacle. Senile gait - small shuffling steps with uncertain, insufficiently coordinated friendly movements of the hands.

sweeping gait- observed in hysterical pseudohemiplegia. The paralyzed leg is dragged with a broom, and does not "rake", describing the arc with the toe, as happens with true hemiplegia.

Neurology. Complete explanatory dictionary. Nikiforov A.S.

Gait- a set of features of the posture and movements when walking. It can be essential in determining the topical diagnosis.

Gait "stork"- with atrophy of the muscles, distal parts of the legs, in particular with neural muscular atrophy of Charcot-Marie (see), the patient sharply bends the hips when walking, raising the hanging feet high.

Gait is atactic- syn.: Cerebellar gait. Walk drunk. A patient with a lesion of the cerebellum walks unsteadily, legs wide apart, steps are uneven in length, while he “throws” from side to side. In the case of a predominant lesion of the cerebellar hemisphere during walking, it deviates mainly towards the pathological focus. The instability is especially pronounced during sharp turns.
Camel gait- gait of patients with torsion dystonia (see), caused by muscle spasms of the spine, pelvis and proximal legs.
Wernicke-Mann gait- see Hemiparetic gait.
Hemiparetic gait- syn.: Wernicke's gait - Mann. It is characterized by excessive abduction of the paretic leg to the side, as a result of which it describes a semicircle with each step (the leg “mows”).
hysterical gait- a perverted, usually changeable gait, not similar to various options its disorders caused by organic neurological pathology. One of its options may be a sweeping gait (see).
Walk "puppet"- the patient walks in small steps (microbasia), while the feet are placed parallel to each other. There is general stiffness, forward tilt of the torso and the absence of arm movements accompanying walking (acheirokinesis). It is observed at parkinsonism (see).

"Fox" gait- the patient, when walking, crosses his legs somewhat, placing his feet on the same straight line. It is observed with lesions of the frontal lobes of the brain.
sweeping gait- syn.: Todd's gait. A gait in which the patient steps over with one leg, and pulls the other, straightened, behind him. Usually a sign of hysteria. Described by the German doctor R. Todd (1809–1860).
Cerebellar gait- a patient with damage to the cerebellum due to ataxia (see) walks uncertainly, legs wide apart. At the same time, if the cerebellar vermis is damaged, it “throws” from side to side, and in the case of a pathological process in the cerebellar hemisphere, it deviates towards this hemisphere. The tendency to fall of the patient is especially pronounced if in the process of walking he makes sharp turns.
Peroneal gait- syn.: Cock's gait. Stamping gait. steppage. With damage to the small tibial nerve, the patient raises his leg high, throws it forward and lowers it sharply. Occurs with peripheral paralysis of the muscles innervated by the peroneal nerve.
Gait "cock"- see Peroneal gait.
Sensitive atactic gait Synonym: Tabetic gait. The manifestation of a violation of proprioceptive (deep) sensitivity is usually associated with damage to the posterior funiculi of the spinal cord.
Len does not feel the position of the legs in space. With preserved muscle strength while walking, the patient looks down all the time and controls the position of his legs with his vision. Due to low muscle tone when walking, hyperextension of the knee joints (genu recurvatum) is manifested, which was noted, in particular, with dorsal tabes (tabes dorsalis). Movements when walking are sharp, steps are accompanied by a popping sound, discrepancy between the length and height of the steps. Difficulties in walking increase sharply in the dark. May be a manifestation of some intravertebral tumors, various kinds spinal cerebellar degeneration, funicular myelosis (manifestation of vitamin B deficiency##12###).
Senile gait- with age, against the background of dyscirculatory encephalopathy, certain changes in gait occur due to the difficulty of maintaining balance. At the same time, while walking, the torso leans forward, the shoulder girdle is lowered, the knees are slightly bent, the arm span decreases (dyadochokinesis), the step is shortened.
Tabetic gait- see Sensory atactic gait.
Todd's gait- see Walking gait.
Trendelenburg gait- as a result of weakness of the muscles that provide abduction of the hip, the patient manifests a skewed pelvis when walking. Usually found in myopathy.
Bilateral Trendelenburg gait- see gait "duck".
Walk "duck" Synonym: Trendelenburg's gait is bilateral. Occurs when the muscles of the pelvic girdle and proximal parts of the legs are affected. The patient shifts from foot to foot when walking. characteristic of myopathy.
Stamping gait- see steppage.

Oxford Dictionary of Psychology

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First described in 1881, Wernicke's encephalopathy continues to be an unrecognized, often misunderstood disease. The cause of Wernicke's encephalopathy is a deficiency of thiamine (vitamin B1).

Occurs from any malnutrition condition, although many physicians mistakenly believe that this disease is unique to alcoholics.

Unfortunately, the syndrome is most often only recognized at autopsy, especially among non-alcoholics. Despite advances in magnetic resonance imaging, Wernicke's encephalopathy remains primarily a clinical diagnosis.

Common clinical findings include mental status changes, ocular dysfunction, and gait ataxia.

Additional characters may be present, 1 or more common results may be missing. Treatment consists of timely intravenous thiamine therapy, and the optimal dose remains controversial.

This review traces the history of Wernicke's encephalopathy from its first description to the current understanding of the disease, including many of the misconceptions, myths, and controversies that surround this disease.

Emergency physicians must be well versed in the varied presentation of Wernicke's encephalopathy because most of the patients end up in the emergency department. In addition, the doctor's knowledge of this disease is vital.

Since the failure to diagnose the results of severe neurological disease leads to mortality, although the treatment is safe and effective.

general information

Because of the catastrophic consequences of undiagnosed Wernicke's encephalopathy (permanent brain damage, death), clinicians should have a high index of suspicion, especially in patients with high risk.
Wernicke's encephalopathy is a clinical diagnosis made at the syndromic level. There are currently no biomarkers that can be used to formulate or confirm a diagnosis.
If Wernicke's encephalopathy is suspected, immediate treatment with an intravenous vitamin is essential, as oral administration is not adequate to prevent permanent brain damage.

Timely administration of adequately dosed parenteral thiamine is a safe, inexpensive treatment for Wernicke's encephalopathy.

Wernicke's encephalopathy is difficult to diagnose and is often treated in clinical practice. The lack of detection and treatment is confirmed by the fact that it is more often diagnosed post-mortem in more than 80% of cases.

Even when it is diagnosed clinically, there are many, often conflicting, recommendations indicating how much it should be given and by which route of administration.

This overview serves as a summary of the diagnosis and treatment of Wernicke's encephalopathy and will help clinicians understand the evidence base to make informed treatment decisions.

Symptoms and signs

Clinical changes occur suddenly. Oculomotor disorders, including horizontal and vertical nystagmus, partial ophthalmoplegia (eg, lateral rectal palsy, conjugate gaze palsy), are common.

Vestibular dysfunction without hearing loss is common, and the external reflex may be impaired. Ataxia as a result of vestibular disorders, cerebellar dysfunction or polyneuropathy; specific gait.

Global confusion is often present; characterized by profound disorientation, indifference, inattention, drowsiness or numbness. Side effects from the peripheral nervous system often increase.

Many patients develop severe autonomic dysfunction characterized by sympathetic hyperactivity (tremor, agitation) or hypoactivity (hypothermia, postural hypotension, syncope). If left untreated, the torpor progresses to coma, then death.

History and etiology

Wernicke's encephalopathy is a neuropsychiatric emergency with high morbidity (84%) and mortality (up to 20%). Wernicke's encephalopathy syndrome from an acute mental state change with concomitant ophthalmoplegia and ataxia was first reported in 1881 by the German neuropsychiatrist Carl Wernicke.

In 1887, the Russian neuropsychiatrist Sergei Korsakov described a syndrome of severe, persistent memory impairment known as.

It has been found, a decade after Wernicke's initial report, that vitamin B1 deficiency is responsible for Wernicke's encephalopathy and Korsakoff's psychosis.

Encephalopathy is associated with acute thiamine deficiency, while Korsakoff's psychosis is associated with chronic thiamine deficiency. Urgent treatment with intravenous thiamine reverses early symptoms.

This is evidenced by the fact that 84% of people who survive an acute episode of Wernicke's encephalopathy, without adequate treatment, develop Korsakoff's syndrome. These data led to the Wernicke-Korsakoff syndrome.

A number of mechanisms can lead to severe vitamin B1 deficiency, although alcohol abuse disorders remain the most common (up to 90%). The estimated prevalence of Wernicke-Korsakoff syndrome is up to 2.8% of the general population, about 12.5%, chronically abuse alcohol.

A recent study found that thiamine inhibits 3H-serotonin uptake (Keating et al., 2004), suggesting that thiamine acts as a neurotransmitter or modulating agent. Its deficiency provokes adverse mood changes and harmful behavior.

Causes

Other causes of thiamine deficiency include gastrointestinal disorders, surgery (eg, gastric bypass), acquired immunodeficiency syndrome, hemodialysis, malignancies, and other systemic diseases.

Thiamine deficiency often results from infection, shock, prolonged malnutrition, or intravenous glucose prior to thiamine in malnourished or alcoholic individuals.

The daily requirement of thiamine for healthy people is related to their carbohydrate intake and ranges from 1 to 2 mg per day. The need increases with alcohol abuse and increased carbohydrate intake. Since the reserves are 30 to 50 mg, it can be assumed that they will be depleted in 4-6 weeks.

Diets are rarely completely devoid of it, on early stages deficiency is corrected by supplementation. However, this route of administration becomes less effective and inadequate as the person consumes more alcohol. Vitamins B6, B1 in food are poorly available for an alcoholic patient with liver disease.

Leevy et al observed morbidly obese patients in the metabolic ward who were maintained on a general level of food and vitamin intake for weight loss. Circulating vitamin levels, including thiamine, were monitored.

As expected, after ∼4 weeks the level fell below the normal range where it remained despite oral administration, indicating that patients are developing malabsorption secondary to their malnutrition.

Pathophysiology

Wernicke's encephalopathy (WE) is an acute neuropsychiatric condition due to an initially reversible biochemical brain injury caused by overwhelming metabolic demands of brain cells that have depleted intracellular vitamin B1.

This imbalance leads to a deficiency of cellular energy, focal acidosis, a regional increase in glutamate, and cell death.

Encephalopathy may result from conditions that cause prolonged malnutrition or vitamin deficiency (eg, recurrent dialysis, hyperemesis, fasting, gastric bleeding, cancer, AIDS). It is sometimes caused by genetic abnormalities that lead to defects in transketolase, the enzyme that processes thiamine.

Certain brain structures are more vulnerable to damage caused by thiamine deficiency, including the thalamus, mammillary bodies, periacusticular, paraventricular regions, the ceruleus locus, cranial nerve nuclei, and the reticular formation.

signs

In fact, the clinical presentation of Wernicke's encephalopathy correlates with the areas of the brain that are affected, resulting in a very variable, non-specific presentation:

Changes in mental status, including stupor, memory impairment, correlate with the dorsomedial thalamus, mamillary bodies, even cortical lesions (poor prognosis).
Wernicke-Korsakoff syndrome is the result of combined thalamo-hypothalamic lesions.
Ocular signs are associated with lesions of cranial nerves III and IV, the ceruleus locus, and the periaqueductive gray area.
Ataxia correlates with lesions of the cerebral cortex.
An affected hypothalamus leads to abnormal regulation of body temperature.

Wernicke - Manna Pose

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Extensive cerebrovascular accident: causes, symptoms, treatment and consequences

A massive cerebral stroke is more likely to occur in people who have already had a local stroke or have experienced recurrent ischemic attacks.

CVA can be caused by blockage or rupture of a vessel

Causes and Contributing Factors

Violation of the blood supply to the brain causes damage to neurons, and this leads to neurological disorders, sometimes to disorders of vital functions, which can lead to the death of the patient. The prognosis for a major stroke is not good, death occurs in 15–25% of cases in the first hours of the disease, after a major stroke, 65–70% of patients remain disabled.

Contributing factors for the occurrence of a massive stroke are:

elevated blood pressure;
cardiovascular diseases;
microstroke or ischemic attacks in history;
diabetes;
atherosclerosis;
bad habits (smoking and alcohol);
obesity;
elderly age.

Types of extensive stroke

Damage to brain cells during a stroke occurs due to a violation cerebral circulation. This can happen for various reasons, the table shows the types of extensive stroke and the pathogenesis of their development:

Symptoms

Symptoms of stroke of various localization

Symptoms vary depending on which part of the brain is affected. The table shows the symptoms that occur when different parts of the brain are affected. The clinical picture for each patient may be different, but there are some signs that correspond to a certain localization of circulatory disorders:

When the process covers both lobes (which is very rare), then both types of symptoms and complete paralysis of the body on both sides can be observed, often the patient develops a coma.

One of the types of extensive stroke is the stem, hemorrhagic type almost always leads to the death of the patient, unless resuscitation is urgently provided, but even in this case the prognosis is unfavorable. A coma usually develops, impaired breathing requires artificial ventilation of the lungs. The consequences of a stem stroke affect all functional areas of a person: hearing, vision, speech, functions internal organs. Most often, the patient remains immobilized and becomes disabled.

The course of the disease

Coma is a fairly common complication of a major stroke.

A massive stroke is often accompanied by a coma, and coma can occur immediately or gradually. Coma in stroke also affects the prognosis of the disease. The longer the coma continues, the worse the prognosis and the more likely the consequences develop.

Coma is a violation of consciousness, when a person stops responding to external stimuli, he seems to fall into a dream, this condition can be observed from several hours to several months. Coma is accompanied by involuntary urination or defecation, impaired breathing and cardiac activity.

Before the onset of a coma, the patient may experience incoherent speech, confused consciousness.

Coma is characterized by a lack of response to bright light, sound, a change in body position, and some of the patient's reflexes, such as reaction to light, swallowing and corneal, can be saved.

Coma in stroke has 4 degrees of severity. A coma of 1-2 degrees gives a significant chance of getting out of it and recovering. At 3-4 degrees, the probability of removing the patient from this state is low, respiratory and cardiac disorders lead to undesirable consequences or death.

Treatment

Drugs used to treat stroke

The principles of treatment for extensive stroke are the same as for local ones:

It is necessary to limit the lesion. Therefore, neuroprotectors are prescribed. With ischemia in the first hours, thrombolytic drugs can help, with hemorrhage, it is necessary to lower blood pressure to optimal values, antihypertensive drugs are prescribed.
Measures are being taken to combat cerebral edema. To do this, use diuretic drugs, plasma-substituting solutions with good rheological properties; osmotic solutions to reduce cerebral edema.

Oxygen therapy is mandatory.
In case of violation of the vital functions of the body, cardiopulmonary resuscitation is indicated.
Patients in a coma may be prescribed parenteral nutrition and vitamin therapy.

Consequences

If the patient has a massive stroke, the prognosis is often poor, only 40% of patients can recover, but they still have certain neurological disorders. In other patients, the consequences of a stroke may be as follows:

Memory violations, they depend on the localization of the process. Both the loss of certain fragments from life and the violation of the perception of new information can be observed. The patient does not remember details.
Speech disorders. The patient has difficulty pronouncing long sentences, speech may not be clear due to muscle damage.
Paralysis, paresis, sensory disorders (paresthesia, numbness) of the limbs. Their distribution also depends on the localization of the acute process, but a patient with a stroke can be easily seen on the street by the Wernicke-Mann symptom (“the hand asks, the leg mows”). This is due to the residual effects after paralysis. The patient has an increased tone of the flexors, so the arm on the side of the lesion is in a half-bent state, and the leg, while walking, seems to describe a semicircle. Central damage to the facial nerves leads to a curvature of the face. The patient cannot show his teeth or smile, the nasolabial fold is smoothed on one side.

Wernicke-Mann Pose and Facial Distortion

Violation of cognitive functions. It is difficult for the patient to concentrate, concentrate attention.
Partial loss of vision, loss of visual fields.
Violation of coordination of movements. It is most often expressed in the form of impaired motor skills of the fingers. It is difficult for the patient to grasp small objects, but sometimes the disturbances are so pronounced that the patient cannot even hold a spoon in his hand.
Urinary incontinence, involuntary defecation.
Epilepsy.
development of dementia.
Death.

Of great importance for such patients is long-term rehabilitation and training in simple self-care skills.

Rehabilitation after a stroke

Useful is physiotherapy, therapeutic exercises, massage. This helps reduce the effects resulting from damage to neurons.

Patients in whom an extensive cerebral stroke caused complete immobility require constant supervision and care. Such patients, in the absence of normal care, quickly die from concomitant complications (pressure sores, congestive pneumonia). Accession of infection, its generalization lead to sepsis and death.

An extensive stroke is much more severe than a local one, and in patients who have had a local stroke, an extensive one subsequently develops in 30% of cases. Therefore, it is necessary to observe preventive measures: monitor blood pressure, get rid of bad habits, lead healthy lifestyle life.

Wernicke Manna Pose for Stroke

I remember my promises from the videos. But for now, it really sucks, I would like to bring down the temperature for at least a couple of days. But for now: "work-home, work-grave." Until then, catch it.

Another chapter. Stroke.

Today we will talk about rehabilitation after a stroke.

The article is not addressed to specialists (they are specialists because they themselves know everything), but to those whose relatives and friends, or themselves, have suffered from a stroke. (I will not consider speech therapy and cognitive problems within the framework of the note - this is not my profile at all.)

A stroke is an acute violation of cerebral circulation. It happens hemorrhagic and ischemic, that is, with or without hemorrhage in the brain tissue. More information is easy to find on the internet.

Standard stroke patient looks like this -

This is the Wernicke-Mann pose (with great difficulty I dug up this classic sketch). "The hand - asks, the leg - mows."

What do we see in this picture. The leg does not bend at the knee, due to the hypertonicity of the quadriceps muscle, on the arm there is hypertonicity of the biceps and flexors of the fingers. It is clear that in this situation a person cannot effectively interact with the outside world.

Rehabilitation consists of three equivalent components. These are support for muscle tissue (solved by massage and other methods of physiotherapy), restoration of motor functions (massage and exercise therapy) and ergonomic support (usually, exercise therapy specialists deal with these issues).

What are the common problems.

First, at the initial stage, the patient has a sharply reduced muscle tone, then hypertonicity begins to increase in certain muscle groups.

Second, the patient has a sharp decrease in volitional impulse. Usually, this occurs against the background of a sharp decrease in blood pressure, which in itself is uncomfortable and causes weakness.

So, we begin to work with the patient.

Rehabilitation should, ideally, begin immediately after transfer from intensive care.

And, yes, I perfectly understand the distance between a conditional 40-50 year old man who was "hit" at work and a 90 year old grandmother who has a history of Alzheimer's and obesity of the III degree.

It is clear that in the first case there is a very good chance for a full rehabilitation, and in the second - no hope. However, even with a "conditional grandma" you can work quite effectively. I had 70+ patients who managed to fully rehabilitate at least to the level of self-service.

The first stage, the development of initial coordination. The problem is that against the background of extremely low muscle tone, there is a global impairment of motor functions. The patient is literally unable to balance even while sitting.

The first task of massage at this stage (and at all subsequent ones) is to restore the conduction of the nerve impulse. This is achieved by means of acupressure. We work on the exit points of the nerve. intense stimulation. No "energetics", just squealing on the nerve. You need to understand that this is not osteochondrosis or there is plexitis - the nerve is quite conductive to ourselves - you need to establish a neural response in the brain. Well, we also remember that in 2-3 minutes the neurotransmitters at the point will “burn out”. Therefore…

The second task is to restore tissue nutrition. Roughly speaking, "pump" the muscles. There is nothing complicated here, the main thing is to catch the moment of increasing hypertonicity, and, accordingly, do a relaxing massage on toned muscles. However, there is a tricky move, you can squeeze the tendon in the upper third, activating the Golgi organ. It works by bypassing the CNS so that the muscle can be temporarily relaxed.

The tasks of exercise therapy for this period are to restore muscle functions as much as possible. Here both medical calculations and supporting positions are used. The minimum task is to teach them to roll over on their own, the maximum is to sit.

The main problem is that I am now describing a certain "vanilla" version.

Very often, the patient enters rehabilitation very late, after 3-6 months. Relatives and friends believed that “it will somehow resolve itself,” and when this did not happen, we get practically a “vegetable” that wants nothing and secretly hates everyone.

The first stage of treatment here is always work with relatives. Miracles do not happen, any recovery is the result of work. Often, teamwork. In the event of a stroke, the involvement of relatives is extremely important. The patient is in dire need of support, but due to the peculiarities of the course of the disease, he is not able to correctly describe his condition.

Then we go on the way of fixing the result. To be honest, I read about ergonomics on Wikipedia. Previously, this by itself was included in exercise therapy. That is, each mastered movement was interpreted as useful. As a matter of fact, it is so. I was able to straighten my arm - you can dress yourself.

Although, of course, some ergonomic assessment of living space is useful. Especially if we have a case with partial restoration of functions. It also happens, unfortunately.

Let me draw some conclusions.

A stroke is not a death sentence. You can restore everything to normal (my father had three strokes - after each he fully recovered).

There are extremely difficult cases. But even there restoration and partial social rehabilitation is possible.

Sometimes they die from it. Two people died of a stroke in the most direct sense before my eyes. And there was simply nothing that could be done. Repeated hemorrhagic strokes, there is a 100% mortality, although resuscitation ... Rather, than a bullet in the head.

Well, the general result.

Stroke is a complex, combined pathology. There is no “uniform” course, as, in fact, there is no treatment. A number of points remain at the discretion of the attending physician, who daily observes the development of the disease.

Perhaps this article is absolutely useless, perhaps it will help someone.

I will reiterate my position. The most effective is early rehabilitation. But there may be categorical restrictions from the attending physician.

Late recovery is a pain! Reimbursement for insurance.

Consequences of a stroke

Hello, dear readers and guests of the site dedicated to neurorehabilitation. Let's talk today and take a closer look consequences of a stroke- ischemic and hemorrhagic, as well as everything connected with this.

Consequences of a stroke.

Violations of any functions after a stroke are directly dependent on its severity, and severity, in turn, on the size of the focus and its location in the brain.

Of course, it would be fair to note that the size of the focus and its localization are far from all factors that determine the persistence of the depth of neurological disorders caused by a stroke, the consequences of which (the nature and severity) can vary greatly, depending on the specific case. What does it depend on?

The degree of dysfunction after a stroke is not always persistent. With a small stroke, the consequences may be minimal or even absent, but this does not happen so often. We will discuss cases when these consequences are present and they are persistent. We will analyze in more detail what exactly the consequences of a stroke are and how they are expressed. Below are the most significant violations of body functions that occur after a stroke.

Right-sided and left-sided hemiparesis after stroke.

One of the most common persistent consequences of a stroke is a decrease in strength in half of the body - hemiparesis. As a rule, after a stroke, there is a decrease in muscle strength in one of the sides of the body, which is opposite to the damaged hemisphere of the brain: if hemiparesis of the left side of the body is a persistent consequence, the stroke occurs in the right hemisphere. By the same principle, hemiparesis of the right side of the body, in which a stroke is observed in the left hemisphere. That is, the focus of infarction in the brain is located in the opposite hemisphere of the affected half of the body.

It also happens that a stroke leads to a complete lack of muscle strength in half of the body, which is called hemiplegia. With hemiparesis, a person experiences difficulty in moving, with hemiplegia, the difficulties are even more significant. Simply put, hemiplegia is paralysis in half of the body ( complete absence movements).

Habitual movements in the body are disturbed, many people have to learn to perform normal daily activities again in order to be able to take care of themselves, be able to eat, change clothes and walk. In general, to do everything that before the illness was considered extremely simple and ordinary to perform. It is the decrease in muscle strength in half of the body that is the main reason for the disability of a person after suffering a violation of cerebral circulation. It is because of this that patients lose the ability to move independently - or lose this ability completely or it is significantly impaired.

As you have already described, gait after a stroke can often be disturbed, while a person begins to move with great difficulty. In some cases, assistive devices may be needed - special walkers, a support cane or a crutch. A characteristic Wernicke-Mann posture develops when walking. Individual parts of the body may be affected without involving the entire half of the body. Depending on the affected half of the body, there are left-sided and right-sided hemiparesis.

Central prosoparesis.

The next, one of the most common consequences, is the so-called central prosoparesis, in which the mimic muscles suffer, resulting in facial asymmetry, as in Figure 1. At the same time, a decrease in strength is observed not in the entire half of the face, but only in its lower part, capturing the mouth, cheek, lips.

The eyelids and eyes with this paralysis of the mimic muscles remain unaffected, despite this, the distortion is quite noticeable and causes discomfort not only during meals or liquids. Central prosoparesis regresses with recovery from stroke.

With central prosoparesis, food intake and fluid intake are difficult. A person experiences obvious discomfort when performing some actions with facial muscles. Habitual emotions are more difficult to express, due to a decrease in strength in facial muscles, sound production is disturbed and speech begins to suffer.

The defect itself brings a tangible inconvenience purely from the cosmetic side. Distortion of the face causes great emotional discomfort, especially when communicating with other people. This can cause isolation and renunciation of communication with others and cause deep depression.

Speech impairment after stroke.

Speech disorders after a stroke are also quite common, at the same time it is one of the very first signs of an onset (upcoming) cerebrovascular accident. Speech impairment is the result of damage to the speech centers of the brain, which is a partial or complete loss of the ability to speak and perceive someone else's speech, called aphasia.

According to statistics, such violations are observed in a quarter of all people who have experienced a stroke, their consequences can be quite persistent. Sometimes it is difficult for a person to speak, due to a violation of the possession of the speech apparatus, and the speech of such people is fuzzy, as if “porridge in the mouth”, and such a violation is called dysarthria . dysarthria more common in stem stroke or localization of this focus in the cerebral cortex. The next speech disorder is aphasia.

Aphasia is the complete absence of speech. Aphasia can be of several types, to name some of them - with the defeat of the speech center responsible for the pronunciation of speech, motor aphasia develops. When the focus of the stroke is located in the center of speech, which is responsible for its perception, the so-called sensory aphasia develops. With sensory aphasia, a person does not understand what is being said to him and does not understand what he needs to answer. If both centers are affected, mixed or sensory-motor aphasia. The "pure" form of aphasia is extremely rare, and with a stroke, it is the mixed form that most often occurs.

There are other types of speech disorders after a stroke, which we will discuss in detail in the following articles on speech disorders. And now let's move on ... In addition to the violations listed above, there are the following consequences of a stroke.

Disturbances in coordination of movements after a stroke.

Impairment of blood circulation in the parts of the central nervous system responsible for the coordination of movements and as a result of a stroke can lead to coordination of movements, which is called ataxia. Disturbances in coordination of movements often occur with stem stroke and this is due to the fact that in the stem part of the brain there are centers for coordinating movements in our body.

There are different degrees of expression. In the most favorable case, these vestibular disorders disappear within the first day after the acute cerebrovascular accident. In other, more severe cases, unsteadiness when walking and dizziness persist for a longer period and may last for months.

visual impairment after stroke.

There may be visual impairments of the most diverse nature. Visual impairment depends on the location of the stroke and the size of the focus. Most often, visual impairment manifests itself in the form of loss of visual fields (hemianopsia). In this case, as you may have guessed, half or a quarter of the visual picture falls out. If a quarter of the picture falls out, it is called a quadrant hemianopia.

Other consequences of a stroke.

Hearing impairments (hypoacusia), smell impairments (hypo-, anosmia), loss of movement skills with the strength stored in them (apraxia) and other disorders that can and should be treated, rehabilitation in this case is very important and should be carried out in a timely manner.
Loss of sensation after a stroke. Violation of sensitivity after a stroke can be of a different nature, but most often it is a loss of the ability to feel pain, recognize heat, cold, and a part of the body as such. It is also possible the appearance of pain syndrome, which is of the most diverse nature and localization. Most often, there is a decrease in sensitivity in any part of the body, this phenomenon is called hypesthesia.

Depression after a stroke.

Depression- another consequence of a stroke that can cross out any efforts of a doctor and loved ones to restore lost functions. According to some reports, up to 80% of stroke survivors suffer from depression in varying degrees of severity. This is a rather serious consequence that can and should be treated.

In addition to the mood for recovery, an additional no less important “bonus” of eliminating depression will be an analgesic effect. It has long been proven that depression can increase pain in a person, and pain in a stroke is not uncommon. Prescribing antidepressants can help with this problem.

It is extremely important to prescribe the “correct” antidepressant, since some of them can cause an “inhibitory effect”, which in some cases can also reduce a person’s desire to follow the doctor’s recommendations and activate for better rehabilitation.

A stroke, the consequences of which remained after a course of treatment in a hospital, is a frequent phenomenon. Such people need a full-fledged rehabilitation course, which often begins already in the hospital. The rehabilitation course itself is prescribed individually, depending on the severity and persistence of the consequences, as well as on the time that has passed since the stroke and the general condition of the patient.

Read about an example of such a rehabilitation center in the article rehabilitation center after a stroke.

Wernicke - Manna Pose

Wernicke - Manna Pose(K. Wernicke, 1848-1905, German psychiatrist and neuropathologist; L. Mann, 1866-1936, German neuropathologist) - a peculiar posture of a patient with central hemiparesis (paralysis), which developed as a result of damage to the internal capsule: bringing the shoulder to the body, flexion of the forearm, flexion and pronation of the hand, extension of the thigh, lower leg and plantar flexion of the foot; due to an increase in muscle tone of the flexors of the arm and extensors of the leg.

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Two months ago I received a burn of the hands and forearms (electronic arc). Now n. Two months ago I received a burn of the hands and forearms (electronic arc). Now on hands, especially on a fold of a brush, contractures were formed. Can they be removed non-surgically? Even on my left hand, my little finger does not fully unbend, the doctor said it will develop, but for three weeks there has been practically no
We picked up a cat with a torn hand, and from the forearm (if possible, vyp. We picked up a cat with a torn hand, and the skin was torn off from the forearm (if I may say so) and the paw bleeds. We sprinkle it with a streptocyte and bandage it, but the paw does not heal. tell me what to do.
I have a congenital absence of a hand, a slightly underdeveloped forearm, maybe l.

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Werbow's symptom

It is characterized by a synergistic unilateral contraction of the gluteal muscles when causing the symptom of Lasegue, as a result of which the buttock on the affected side rises. It is noted with a unilateral lesion of the sciatic nerve. On the healthy side, as a rule, is absent.

Vernet-Sycorecolle (villare) syndrome

It consists in the defeat of the IX, X, XI and XII cranial nerves and the upper cervical sympathetic ganglion.

Vernet torn hole syndrome

It is characterized by damage to the IX, X, XI cranial nerves exiting through a torn hole. Damage symptoms: difficulty swallowing dense food; the back wall of the pharynx is moved to the healthy side; violation of taste on the back of the root of the tongue; decreased sensitivity of the soft palate, mucosa of the posterior pharyngeal wall and larynx; urge to cough, pseudoasthma and salivation; on the side of the focus of paresis of the soft palate, larynx, sternocleidomastoid and trapezius muscles.

The syndrome is most often caused by diseases of the submandibular salivary glands, phlegmon, phlebitis, meningitis, tumor and other processes on the base of the skull in the region of the laceration. Described by YVernet in 1916.

Werner syndrome

It is characterized by small stature, a relatively large skull, a beak-shaped nose, a small mouth with a large chin (“bird’s face”), thin upper and lower limbs, especially in the distal sections, early atherosclerosis, cataracts, skin atrophy (especially of the legs and feet) with the development of trophic ulcers, a mask-like face (sclerodermic type), hypogenitalism (violation of menstrual cycle, sterility, high timbre of voice, delay or absence of secondary sexual characteristics), dysfunction of the parathyroid glands (calcium metabolism disorder), thyroid gland (osteoporosis), sometimes dementia.

Premature graying and baldness are noted. The syndrome is caused by congenital endocrine insufficiency. Described by the German physician O. Werner in 1904.

Werinke-Mann (type of contractures, Wernicke-Mann position) syndrome

It is observed in pyramidal lesions. On the upper limb, the muscles that raise the girdle of the upper limb, abduct and rotate the muscles of the shoulder, extensors and supinators of the forearm, extensors of the hand and fingers of the hand are more often affected, on the lower - muscle groups that abduct and adduct the thigh, muscle groups that flex the knee and foot.

When the flaccid stage of heminlegia is replaced by a spastic one, the antagonists of these muscle groups are especially hypertonic. Spasticity, if it is sufficiently pronounced, leads to the formation of contractures.

As a result, the upper and lower limbs assume the following position: the belt of the upper limb is lowered, the shoulder is adducted and rotated inwards, the forearm is pronated and bent at the elbow joint, the hands and fingers are bent, the thigh is extended and adducted, the lower leg is unbent, the foot was in the position of pes varoquinus, therefore paralyzed lower limb as if it becomes somewhat longer healthy. In order not to touch the floor while walking, the patient, not being able to raise the limb up, “mows” it, that is, takes it to the side, describing a semicircle with the foot (“the hand asks, the leg mows”).

The Wernicke-Mann position is often observed with lesions of the pyramidal tract in the region of the posterior crus of the internal capsule. Described by German neuropathologists K. Wernicke in 1889 and L. Mann in 1896.

"Handbook of Neurological Semiology",
G.P. Lip

Schwabach test It is carried out using a sounding tuning fork, which is placed on the mastoid process on the side of the investigated vestibulocochlear organ and the duration of bone conduction of sound is determined. The obtained value in seconds is compared with the bone conduction of the patient's unaffected vestibulocochlear organ or with the conduction in healthy person. When the sound-conducting apparatus is damaged, bone conduction is lengthened, and when the sound-receiving apparatus is damaged, it is shortened. Shvetsova…

Schilder's test During the test, the examiner, standing with his eyes closed, stretches his upper limbs forward. With a sharp turn of the head to the side, the lower limb slightly rises on the same side, and both upper limbs deviate somewhat in the same direction. The change in the position of the upper limbs is especially pronounced in cerebellar processes. Described by the German psychiatrist P. Schilder in 1912 ....

Barbell test (test for the duration of breath holding) It is determined by the following method: after two deep breaths and exhalations, a calmly lying patient is offered to take an intensified breath and hold his breath for as long as possible, holding his nose with his fingers. The duration of breath holding is determined by a stopwatch. Similarly, the time of holding the breath during exhalation is noted. Between determining the duration of the delay on inhalation and exhalation ...

Shcherbak's (thermoregulation) reflex Method of inducing the reflex: the patient's rectal temperature is determined, after which his upper limb is immersed for 20 minutes in water at a temperature of 32°C. Then, over 10 minutes, the water is gradually heated to 42°C and the rectal temperature is measured again immediately after heating and after 30 minutes. With the preserved function of thermoregulation immediately after warming the limb ...

Edelman's symptom Is a painful topical reflex. It consists in extension of the big toe when causing Kering's symptom. It is observed in diseases accompanied by irritation of the membranes of the brain and spinal cord. Eddie's syndrome It is characterized by peculiar reactions of the pupils: when illuminated, the pupil does not narrow, but expands in the dark; under the influence of light, it slowly narrows again (moreover, it becomes narrower than before the test) and ...

WERNIKKE-MANN POSE

(K. wernicke, 1848-1905, German psychiatrist and neuropathologist; l. mann, 1866-1936, German neuropathologist) a peculiar posture of a patient with central hemiparesis (paralysis) developed as a result of damage to the internal capsule: bringing the shoulder to the body, flexion of the forearm, flexion and pronation of the hand, extension of the thigh, lower leg and soles foot flexion; due to an increase in muscle tone of the flexors of the arm and extensors of the leg.

Medical terms. 2012

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