Theme:

Theme: Autonomic nervous system (peripheral and segment parts, Hypothalamus, Limbic-Reticular system).

Special Clinical Examinations of Diseases of Nervous System

 

 

The Autonomic nervous system. Anatomy. Functions.

The symptoms of lesion

 

The autonomic nervous system is a part of nervous system that regulates the activity of internal organs, glands, blood and lymphatic vessels, smooth and striated muscles and organs of sensation.

      The modern physiology defines Autonomic nervous system as a part of nervous system due to which the activity of internal organs and metabolism is regulated. 

      The autonomic nervous system is a purely efferent system of nerve fibers with ganglia and plexuses outside the central nervous system in­nervating the blood vessels, heart, viscera, glands, and smooth muscles throughout the body. Although afferent nerve fibers conveying im­pulses from these structures to the central nervous system are present in autonomic nerves such as the vagus and the splanchnic nerves as well as in peripheral somatic nerves, they are considered separate from the autonomic nervous system. These visceral afferent nerve fibers are thinly myelinated or nonmyelinated and the impulses they carry are related to visceral sensations, such as pain and distention, and to vis­ceral reflexes underlying functions such as respiration, maintenance of blood pressure, and micturition. Their cells of origin are in spinal dor­sal root ganglia and in certain cranial nerve ganglia. The visceral af­ferent fibers terminate in the spinal cord and brain stem oeurons subserving local visceral reflexes and oeurons forming secondary visceral tracts. In the spinal cord these visceral tracts probably exist as multiple chains of neurons, crossed and uncrossed and not well de­fined into specific tracts, in the lateral columns of white matter near the ventral horns.

There is a close connection and similarity between the autonomic and somatic nervous system.

• The morphological and functional unit of both of them is a neuron

• The main functional unit is a reflex arch.

• The autonomic nervous fibers go within cranial nerves and spinal nerves.

 

Anatomy

The autonomic nervous system is divided into such parts:

• Central (all the structures that are within the brain and spinal cord)

• Peripheral (all the others structures)

 

    The central autonomic nervous system is divided into:

        above – segmental level (the limbic system, reticular formation, hypothalamus)

        segmental level

The last one according to the structure and functional peculiarities is divided into sympathetic and parasympathetic nervous system.

 

The peripheral part of autonomic nervous system is presented by:

        The nodus of Ashof – Towar

        The plexus of Meisner and Auerbach

        Sympathetic noduses

        Solar and hypogastrical plexuses

        White and gray fibers

 

Anatomically, the autonomic nervous system consists of two divi­sions:

1. cranial-sacral (parasympathetic) outflow

 2. thoracic-lumbar (sympathetic) outflow

Arising from nerve cells in the midbrain, medulla oblongata, and the second, third, and fourth seg­ments of the sacral spinal cord, the preganglionic parasympathetic fibers synapse in ganglia which are outside the central nervous system and located close to, or in, the structures they supply. The pregan­glionic sympathetic fibers arise from nerve cells in the intermediolateral column of gray matter in spinal cord segments Thl through L2, and they synapse in the two paravertebral sympathetic ganglionic chains and in the several prevertebral ganglia (celiac, superior and inferior mesenteric and aortic). Preganglionic nerve fibers are myelinated; postganglionic nerve fibers are not.

The cranial portion of the parasympathetic outflow consists of nerve fibbers carried in the third, seventh, ninth, and tenth cranial nerves.

The sacral portion of the parasympathetic outflow arises from nerve cells located in the intermediolateral zone of gray matter of the second, third, and fourth sacral segments of the spinal cord.

 

There are two main functions of autonomic nervous system.

        Ergotropic (homeokinesis) – adjustment to the changes of environment and providing the needs of the organism.

        Trophotropic (homeostasis) – it supports the constant internal reactions and provides anabolic processes.

 

The limbic system was described by French neuro – anatomist Broka in 1878. Mc Lein continued its studying in 1952. It consists of:

        Bulbus olphactorius, tractus olphactorius, trigonum olphactorii, substantia perforata anterior

        Septum pellucidum

        Gyrus cinguli

        Gyrus hypocampalis

        Orbital part of frontal lobe

        Corpus amygdaloideum

        The pole of temporal lobes

 

Function

1.      Emotional reactions

2.      The reception of afferent impulses from internal organs

3.      It is a memory substratum; it preserves information about previous genetically inherited experience

4.      It provides motivation to thirstiness, hunger, sexual desire

5.      It regulates the state of sleepiness and liveliness

6.      It indirectly regulates the function of internal organs

 

 

The symptoms of lesion

1.      Emotional disturbances.

2.      Anorexia or bulimia.

3.      Sleeping disorders.

4.      Sexual disturbances.

5.      Memory disorders.

 

The lesion of temporal lobe leads to the changes of eating behaviour. For example mice catch and put into the mouth different objects and even snakes in spite of the fact that normally they are afraid of snakes.

The lesion of corpus amygdaloideum leads to increasing of appetite and obesity (the experiment was held on cats).

Hypersexuality was noticed in experiments in spite of the animals’ family and sex.

The lesion of gyrus cinguli is associated with memory disorders especially on current events. All these events are forgotten in 2 – 3 min. But those events that are associated with emotions, visual, smell, auditory influences are much more stable.

The irritation of some structures leads to aggression.

 

Reticular formation

      It is a tonus motor of the brain, which works constantly in the brain stem. It was described by Deiters, Bechterev, and Ramon & Kachal. It consists of great number of cells, the axons of which are going in different directions and create a reticule.

      In spite of the other cells of nervous system the cells of reticular formation accept pain, light, temperature and humoral impulses and send them to the brain cortex.

      Thus the main functions of reticular formation are:

        To support the brain cortex tonus, its state of liveliness which is necessary for the normal activity. The reticular formation energizes the brain.

        It supports the certain level of activity of autonomic centers (the activity is very similar to that of sympathetic nervous system. There is also the same mediator – noradrenalinum)

 

Function

1.      The control of sleepiness and liveliness.

2.      To accept the information from the environment.

3.      To keep in tonus all the forms of behaviour, those have long – lasting character.

 

The symptoms of lesion

        The low activity of RF – the patient is unconscious.

        Decreased activity of RF – sleepiness.

      The lower parts of RF have general and long – lasting influence on consciousness and behavior, the upper ones have short – lasting and specific influence.

 

Hypothalamus

      Hypothalamic region has 32 pairs of nuclei of cranial nerves. They can be divided into three groups.

        Anterior – it is associated with parasympathetic function

        Middle – endocrine – trophic

        Posterior – has mainly sympathetic influence.

 

The peculiarities of activity:

1.      Motor cortex receives 440 capillaries per 1 mm³, visual cortex – 900/mm³, hypothalamic region – from 1650 to 2600/mm³.

2.      Almost all the arterial brain systems give their branches to hypothalamic region. That makes impossible disturbances of its activity.

3.      There is no space of glia between the vessels and gangliocytes. That provides quick reaction to the changes of internal surroundings.

      Hypothalamus is closely connected with cortex, thalamus, extrapyramidal nervous system, nuclei of brain stem and spinal cord, reticular formation and hypophysis.

 

The function of hypothalamus

1.      Regulation of heart – vascular activity

2.      Regulation of lipid, water, mineral metabolism

3.      Thermoregulation

4.      Regulation of vessels’ and tissue membranes penetrance

5.      Regulation of endocrine glands’ function

6.      Constant internal surroundings support

7.      Adaptation

8.      Biorhythm

9.      Emotional behaviour

 

      Hypothalamus rules the internal world by means of three ways:

        Through the nervous impulses

        Humoral

        Hormonal

 

The very important role belongs to the releasing factors. In hypophysis there are 7 tropic hormones that activate the production of certain hypophysis hormone:

• Corticoliberinum

• Tirioliberinum

• Luliberinum

• Foliliberinum

• Somatoliberinum

• Prolactoliberinum

• Melanocytoliberinum

There are 3 inhibiting hormones:

• Prolactostatinum

• Melanocytostatinum

• Somatostatinum

 

Hypothalamic syndromes are those that are associated with the lesion or deficiency of hypothalamus.

 

1.      Autonomic – vascular – visceral – is associated with crisis of paroxysmal character.

        Sympathetic – adrenal

        Vago – insular

        Mixed

2.      Neuro – endocrine – metabolic – is associated with increasing or decreasing of hypophysis function (Itsenko – Kushing, acromegaly, early climax, impotence, non sugar diabetes, tyreotoxicosis).

3.      Neuro – trophic is associated with trophic disturbances (dryness, neurodermitis, ulcers, bed sores, acute perforates of stomach and esophagus).

4.      Neuro – muscular – hypothalamus provides chemical and biochemical activity of extrapyramidal nervous system and cerebellum.

        Myasthenia

        Myotonia

        Paroxysmal myoplegia

5.      Thermoregulation disturbances – the temperature is 37,1 – 37,5, there is asymmetry under the arms, in the mouth and in rectum. Sometimes this symptom has paroxysmal character and is associated with trembling.

6.      Sleeping disorders

        Insomnia

        Lethargy (a special form – narcolepsy) – sudden attack of sleepiness that can happen in any place and position of the patient. Sometimes they are associated with catalepsy (the loss of muscle tonus)

        Sleeping inversion

 

Parasympathetic nervous system is presented by:

        Mesencephalic level (nuclei of Perlea and Yakubovich), the fibers are going within the III CN and provide innervating of m. Sphincter pupillae, m. Ciliaris

        Bulbar (n.salivatorius superor et inferior, n. dorsalis nervi Vagi) within VII, IX, X CN’s innervate parotid, sublingual, submandibular glands and internal organs (except the pelvic organs)

        Sacral part – the cells of lateral horn S2 – S4 – innervating of pelvic organs.

 

There is the arch of pupil reflex on mesencephalic level. The symptoms of lesion are:

          Spasm or paralysis of accommodation

          Mydriasis

          Direct or indirect symptom of Argil – Robertson

 

The symptoms of lesion of bulbar level:

1.      Salivation or xerostomy

2.      Tears or xerophthalmy

3.      Dyspnoe, Biot, Chein – Stocks types of breathing

4.      Tachycardia, arterial hypertension, arythmia, asystoly

 

 

 

Sympathetic nervous system consists of the cells of lateral horn of spinal cord from C8 to L2. The axons within the anterior roots leave the spinal cord. Some of them are finished in sympathetic trunk (it consists of 20 – 23 noduses) – 3 cervical, 10 – 12 thoracic, 3 – 4 lumbar, 4 pelvic. The rest fibers are going to the prevertebral noduses or plexuses.

Common features:

1.      There are 2 neurons. The second neuron is located in ganglion

2.      Preganglionar fibers are myelin –associated.

3.      Postganglionar fibers are without myelin.

 

Differential features:

1.      Mediator

Sympathetic nervous system – adrenalin, noradrenalin

Parasympathetic nervous system – acetylcholine

2.      The length of fibers

Sympathetic nervous system – short pre- and long postganglionar fibers

Parasympathetic nervous system – long pre – and short postganglionar fibers

 

  Symptoms of lesion

1.      The lesion of lateral horns of spinal cord:

        Autonomic – vascular (pale, cyanosis)

        Trophic (edema, arthropaty)

        Secreting (dryness of the skin, hyperhydrosis)

C8 – Th3 – head and neck

Th4 – Th7 – shoulders and arms

Th8 – Th9 – body

Th10 – L3 – pelvis and legs

 

2.      The lesion of segments of the spinal cord – S3 – S5

        Retention of urine

        Truly urine incontinence

        Ishuria paradoxa

 

3.      The lesion of upper cervical sympathetic nodes:

        Causalgia

        Paresthesia, hypesthesia

        Vasomotor, secreting, trophic disorders in head and neck region

        Horner syndrome

 

4.      The lesion of Nodus stellatum:

          Causalgia

          Paresthesia, hypesthesia

          Vasomotor, secreting, trophic disorders in head and neck region

 

      5. The lesion of upper thoracic noduses:

          Cardialgia

          Tachycardia

          Breathing disorders plus all the above named symptoms.

 

      6. The lesion of Lower thoracic and lumbar noduses:

        Visceral and autonomic disorders of the organs of abdominal cavity.

 

7. The lesion of Solar plexus:

        Dull pain in the abdomen

        Increased aorta pulsation

        Instable AP

        Instable stool

        Poli – oligouria

        Glucosuria

 

     8.  The lesion of Posterior neck sympathetic nodus:

          Neck pain like “casque putting off”

          Photopsia

          Vestibular syndrome

 

The disturbance of vegetative functions:

1.            The paroxysmal signs

Sympathy-adrenal attacks:                         Vagoinsular attacks:

a)     skin is pail                                            a) hyperemia

b)     xerostomia                                       b) hyperhidrosis

c)      dryness of hair and skin                   c) oily skin and hair

d)     tachycardia                                      d) bradycardia

e)     high blood pressure                         e) low blood pressure

f)        midriasis and widing of                   f) miosis

     eye-slit                                              g) angina pectoris

g)     exophthalmia                                   h) salivation

h)      tremor                                              i) breathlessness

i)        gooseflesh                                        j) abdominal spastic pain

                                                                     k) diarrhea,

l)                                           frequent and abundant urination

 

                                            2. The lesion signs:

a)     periarthritis                                        a) incontinence of urine and feces

b)     epicondilitis                                       b) ischuria /retention of urine

c)      miositis                                              c) eye accommodation paralysis

d)     hyperkeratosis                                   d) midriasis

e)     fissures of skin                                  e) breath

f)        arthropatias                                       f) dyspnea

g)     trophic ulcer                                      g) apnea

h)      alopecia                                             h) cardiac arrhythmia

i)        hyperpigmentation                             i) asystolia

j)        Horner’s sign                                     j) collapse

(ptosis, miosis, enophthalmia)

 

 

Methods of investigation of autonomic nervous system

      There are numerous clinical, laboratory and instrumental methods of investigation of ANS. The choice of the method depends on our aim.

      First of all we start with investigation of present state of ANS. For this purpose different tables are used.

      Normally there is a balance between the sympathetic and parasympathetic nervous system. But it can be changed in different periods of our life. 

   

There are five types of neurologic disorders of urination and urinary bladder control:

1.     The centrally uninhibited bladder

2.     The sensory paralytic bladder

3.     The motor paralytic bladder

4.     The automatic reflex bladder

5.     The autonomous bladder

 

The centrally uninhibited bladder functions well in respect to emp­tying; but urgency, frequency, and incontinence are common. This type of disorder occurs especially in elderly people and is attributed to diffuse brain disease with resultant inadequate control over the primitive mic­turition reflex. It is often confused with the symptoms of prostatism.

 

The sensory paralytic bladder results from peripheral or radicular sensory denervation. The bladder becomes atonic, loses the feeling of distention or the elicitation of reflex emptying, and gradually retains a significant amount of residual urine. This condition occurs in tabes dorsalis, diabetic neuropathy, and the combined-system disease of pernicious anemia.

 

The motor paralytic bladder is also atonic but is due to neuronal loss in the S2-4 segments or their axons in the parasympathetic outflow. Poliomyelitis and trauma to the conus medullary may produce this syndrome.

The automatic reflex bladder is a consequence of spinal cord disease above the S-2 level (e.g., trauma, compression, multiple sclerosis) in which local reflex arcs are intact. The sensation of fullness is impaired or lost. Frequency, urgency, incontinence, incomplete emptying, and and the inability to void are the usual symptoms. Though micturition may be possible with incomplete cord lesions, urinary tract damage may still result from ureteral reflux or infected residual urine.

The autonomous bladder has no neural connection on either side of the reflex arc and functions imperfectly on a myogenic basis. An atonic bladder with secondary overflow incontinence and impaired drainage of the upper urinary tract is characteristic.

 

The pupillary reactions. Normally the pupils are round and equal in diameter. Normal pupils are small in sleep and dilate with arousal. Difference in size (anisocoria), if small, may not represent disease and can be evaluated accurately only with reference to other findings, such as ptosis. Pupillary diameter is chiefly dependent on intensity of illumination but is greater in children than in adults and is usually small in the elderly. In ordinary room light the diameter may vary from 2 to 6 mm. The pupillary size results from the balance between sympathetic and parasympathetic innervation.

Fibers carrying impulses resulting from light stimulation of the retina (the afferent side of the reflex arch), both crossed and uncrossed, traverse the optic tract and bypass the lateral geniculate body to synapse in the pretectal region of the midbrain. Here another crossing is made they further ensures that stimulation of one eye will cause the contralateral as well as the stimulated pupil to constrict—the consensual reaction. The pupil of a blind eye will not constrict when its retina is exposed to light. But it will do so when the other, normal eye is stimulated.

The efferent limb of the reflex originates in the Edinger-Westphal nucleus, a part of the third-nerve nucleus. The pupillomotor fibers course with other fibers of the third cranial nerve to synapse again in the ciliary-ganglion, from which terminal fibers innervate the iris and ciliary body.

When the pupils are unequal in size (anisocoria), either or both may be abnormal. The larger pupil may react poorly to light as a result of a partial third-nerve paralysis, or the smaller pupil may be part of Horner’s syndrome. When anisocoria is present it is important to examine the pupils in both light and dark. The difference in pupillary size in Horner’s syndrome will increase in dark, whereas that due to partial third-nerve paralysis will increase in light.

 

Horner’s syndrome, when complete, is characterized by:

1.      ptosis of the upper lid,

2.      miosis,

3.      loss of sweating on the same side of the face.

4.      pupillary reaction to light is normal, but the pupil does not dilate to psychosensory stimuli such as a loud noise.

 The syndrome may be pro­duced by a central or peripheral lesion and may be partial or complete. The importance of the syndrome derives from the vulnerability of the sympathetic pathways at different points in their long course (see above). Associated signs can help locate the level of a lesion after Horner’s syndrome has betrayed the interruption of pathways.

The Argyll Robertson pupils of tabetic neurosyphilis are small (miotic), irregular, and often unequal in size. They react little or not at all to light but constrict promptly when the eyes converge on a near object. A similar dissociation between the light reaction and the near response may be seen in patients with diabetes, encephalitis, and midbraieoplasm.

 

There are Trophic disorders:     

 

 

 

 

Students’ practical Study Program.

I step. Aim: To determine presence of signs of vegetative system lesion. For this purpose it is necessary:

 

The scheme of diagnostic search of vegetative disorders

I.         To gather an anamnesis and to examine patient’ status.

II.       At the analysis of the complaints of the patient to find out presence of attributes of a lesion of a vegetative system:

a.      activity of inner organs (attacks of tachy- and bradycardia, breath, dyspeptic disturbance after meals, abdominal spastic pain, diarrhea, frequent and abundant urination),

b.      activity of cardiovascular system (attacks of a skin pallor and hyperemia, high and low of blood pressure),

c.      activity of the sweating, sebaceous glands and lacrimal organs (salivation, hyperhidrosis, dry skin, eyewatering, xeroftalmia),

d.      activity of pelvic (urogenital) organs (ischuria /retention of urine/, incontinence of urine and feces),

e.      trophic disturbance (hyperkeratosis, skin lesion, peeling of the skin, fissures of skin, pustules, skin edema, hyperpigmentation, alopecia, hemiatrophia, osteoarthropathia),

f.        disturbance of height and substances exchange (low and high height, increasing of weight, cachexia, acromegalia),

g.      disturbance of sleep, thermoregulation, memory, emotions and tendencies.

 

II step. Aim: To determine part of vegetative nerve system (sympathetic, parasympathetic) lesion. Make a conclusion about presence of pathology of sympathetic or parasympathetic part of vegetative nervous system.

III step.  Aim: To find level of lesion vegetative nervous system.

IV step. Aim: To make topical diagnosis of a pathological process level localization in vegetative nervous system. In topical diagnosis it is necessary to point main vegetative signs (syndromes), the character of vegetative pathology.

 

 

 

 

Special Clinical Examinations of Neurological Patients

(Electromyography, Echo-Electroencephalography, Electroencephalography, CT-scan, Pneumocephalography, Cerebral Angiography, Roentgenography, Reoencephalography, MRI).

 

Electroencephalography  (EEG)

 

The EEG involves recording of the spontaneous electric activity of the brain from the scalp and activity elicited by activation procedures. The amplitude of EEG activity recorded by the scalp electrodes is generally about 10 to 60 microvolt. Usually, the EEG is sampled simultaneously from 8 to 16 pairs of electrodes in selected combinations (montages). The most characteristic feature of the normal EEG of an adult during relaxed is the alpha rhythm (8 to 12 Hz – rate, 100 mV – amplitude) and the beta rhythm (14 to 40 Hz, 15 mV). The pathological rhythm is the delta (less than 3 Hz) and theta (4 to 5 Hz) 

Ambulatory electroencephalography (AEEG) monitoring is a relatively recent technology that allows prolonged electroencephalographic (EEG) recording in the home setting. Its ability to record continuously for up to 72 hours increases the chance of recording an ictal event or interictal epileptiform discharges. AEEG is a less expensive alternative to inpatient monitoring, with costs that are 51-65% lower than a 24-hour inpatient admission for video/EEG monitoring.

Continuous cardiac monitoring was first described by Holter in 1961. The development of portable EEG recording proved more problematic than the Holter monitor because of the need for signal amplification and multichannel recording. A multichannel portable recorder was developed in the early 1970s. This technology was later adapted to EEG recording, and miniature preamplifiers that could be worn on the head were developed.

Early clinical investigations documented the ability of AEEG to record identifiable focal and generalized epileptiform activity. In 1982, Ives introduced a 16-channel AEEG that utilized signal multiplexing. The 16 channels allowed improved spatial resolution and localization but recorded discrete samples rather than continuous EEG.

In 1983, a cassette tape AEEG system was introduced; it used off-head preamplifiers that had continuous 8-channel recording capability, real-time identification, and gain and filter adjustments.

In the past decade, computer technology has enabled portable recording of up to 36 channels with sampling rates of up to 400 Hz. Currently, numerous AEEG systems are available commercially (see the image below).

 

Components of an ambulatory EEG system.

Indications

AEEG has several important clinical applications. Depending on the clinical suspicion, other diagnostic tests (eg, ambulatory cardiac monitoring, polysomnography [PSG] or inpatient video/EEG monitoring) may be more appropriate in a given situation.

Confirmation of clinical suspicion of epilepsy

A clinical suspicion of epilepsy can be confirmed by recording a seizure on AEEG. This is most likely to occur when the patient is experiencing daily or almost daily spells. Studies looking at the diagnostic yield of AEEG indicate that 6-15% of AEEGs record seizures.

Higher yields have been reported from 16-channel AEEG with computer-assisted seizure detection than from older 4- or 8-channel systems without seizure-detection algorithms. A 2001 study in which 502 patients were evaluated with computer-assisted 16-channel AEEG demonstrated that 8.5% of patients had a seizure during the recording period (mean, 28.5 h).

In patients with intractable epilepsy, AEEG has been used to localize seizure onset as part of presurgical evaluation. However, inpatient video/EEG monitoring remains the standard for presurgical evaluation.

Evaluation of interictal epileptiform activity

Detection of interictal epileptiform abnormalities in the absence of recorded seizures can provide supporting evidence for a clinical diagnosis of epilepsy.

Studies have demonstrated that 34.9% of patients with known seizures had a positive AEEG, whereas 15.3% of 216 patients in whom the diagnosis of seizures was considered (ie, patients with episodic alterations of behavior, perception, sensation, or motor functioning) had interictal epileptiform abnormalities on 4-channel AEEG. When a 16-channel recorder was used, 38% of patients who were referred for AEEG had some type of epileptiform abnormality.

AEEG is highly specific; spikes were found on overnight AEEG in only 0.7% of asymptomatic adults without a history of migraine or a family history of epilepsy. In patients with a history of migraine headaches and those with a family history of epilepsy, the incidence of spikes on AEEG was 12.5% and 13.3%, respectively.

Some patients in whom epilepsy is suspected have a normal routine or sleep-deprived EEG. In these patients, AEEG can increase the chance of detecting an epileptiform abnormality. Of patients who previously had normal or nondiagnostic routine EEG, 12-25% have epileptiform activity on AEEG.

A study comparing the usefulness of sleep-deprived EEG and computer-assisted 16-channel AEEG in patients with suspected epilepsy (but a nondiagnostic initial routine EEG) found that sleep-deprived EEG improved detection of epileptiform discharges by 24%, whereas AEEG improved detection by 33%. Of the 46 patients studied, 15% had actual seizures recorded on AEEG, and none had seizures during the sleep-deprived recording.

Patients may have epilepsy without interictal epileptiform abnormalities on EEG, but this occurs in fewer than 20% of patients. In a study using a 4-channel recording system, 3 patients had only seizures recorded without interictal abnormalities. AEEG with 16 or more channels increases the probability that interictal epileptiform abnormalities will be found.

Documentation of seizures of which patients are unaware

For a patient to have seizures and yet be unaware of them is not uncommon. Brief alterations of awareness occur in both absence and complex partial seizures. AEEG is helpful at identifying seizures that are unrecognized or unreported by the patient.

Absence seizures may be so brief that the patient is unaware of them. A study using AEEG to evaluate absence seizures in pediatric patients found that most paroxysms of generalized spike and wave discharges (see the image below) were asymptomatic.

An 8-second burst of generalized 3-Hz spike and wave captured on an ambulatory EEG.

Patients with complex partial epilepsy are often amnestic for their seizures. The sequelae of a nocturnal generalized convulsive seizure, if present at all, may be so subtle (eg, fatigue, muscle soreness) that the patient is unsure whether a seizure actually occurred.

A study of patients in an epilepsy monitoring unit found that 63% of all seizures were unrecognized by the patients. This difficulty in identifying the occurrence of seizures impedes seizure diagnosis and assessment of treatment adequacy.

Liporace et al found that the AEEGs of 3 patients (of 46) demonstrated seizures that were not designated as events by the patients.^[24] Tatum et al found that more than one third of AEEGs with ictal activity contained at least one seizure that was unreported by the patient. These studies demonstrate the utility of AEEG at capturing unsuspected events.

Evaluation of response to therapy

Because a significant number of patients are unaware of their seizures, responses to treatment are frequently difficult to gauge. Patients with mental retardation or other forms of encephalopathy may be unable to report seizures accurately. In such cases, AEEG can have a significant impact on clinical management.

AEEG is particularly useful in quantitating response to the treatment of absence seizures. If untreated, such seizures typically occur numerous times per day; adequate treatment usually normalizes the EEG.

Evaluation of nocturnal or sleep-related events

Certain diagnoses are difficult to confirm with the typical 20-minute outpatient EEG. The interictal epileptiform discharges of benign rolandic epilepsy, for example, are highly activated by sleep and may not always be achieved adequately in a laboratory. Continuous spike and wave activity during slow-wave sleep is another entity that may demonstrate a relatively normal EEG during waking hours and a strikingly abnormal EEG during deep sleep.

Because of its capacity to record an entire night of sleep, AEEG is invaluable in assessing these clinical situations. Another advantage is that children can be monitored at home.

If a nonepileptic sleep disorder is suspected, PSG is the preferred study because of the added information from monitoring electromyography (EMG), eye movements, electrocardiography (ECG), and respiration.

The history may not differentiate clearly between a sleep disorder and epilepsy. AEEG may record frequent arousals (suggesting sleep apnea) or decreased rapid eye movement (REM) sleep latency (suggesting narcolepsy). In a study of 500 patients who had AEEG, narcolepsy was suggested in 6 patients, including 3 in whom narcolepsy had not been suspected.

Evaluation of suspected pseudoseizures

Pseudoseizures, also known as psychogenic seizures or nonepileptic events are clinical events in which patients perceive altered movement, emotion, sensation, or experience similar to those due to epilepsy but without an electrographic ictal correlate.

Pseudoseizures are surprisingly frequent, occurring in as many as 20% of patients at epilepsy referral centers and in 5-20% of outpatient populations. Some patients have both pseudoseizures and epileptic seizures; coincident events occur in an estimated 10-60% of epilepsy patients.

AEEG can be a useful screening tool in identifying patients who have nonepileptic paroxysmal events. In one study, 36% of patients had event marker activations without associated electrographic changes.

Potential problems exist in using AEEG to definitively diagnose nonepileptic seizures. A 24-hour recording without associated video does not allow evaluation of clinical stereotypy, which is valuable when evaluating patients with unusual seizure manifestations and minimal EEG changes. Scalp EEG may not show electrographic ictal abnormality during some frontal lobe seizures or may show only subtle abnormalities that would be difficult to interpret without associated video.

Kanner et al found that 25% of their group of 12 patients with supplementary motor seizures demonstrated no electrographic ictal pattern during seizures.

Seizures and nonepileptic seizures may be associated with movement and muscle artifact that may obscure the underlying EEG. Although AEEG may be a useful initial screening tool for nonepileptic events, inpatient video/EEG monitoring remains the criterion standard in evaluating nonepileptic seizures.

Evaluation of syncope

AEEG may be helpful in evaluating syncope or near-syncope if an ECG lead replaces 1 of the EEG channels.^[34] If cardiogenic syncope is suspected, a Holter monitor or prolonged cardiac event monitor may be more useful clinically. Although arrhythmias have been diagnosed with continuous ambulatory EEG/ECG recording, a study of epileptiform abnormalities in AEEG found that only 1 of 67 patients with syncope, near-syncope, or episodic dizziness had an epileptiform abnormality.

Future applications

Seizure anticipation methods are under development to identify EEG changes before seizure onset, allowing ongoing assessment of the probability of seizure occurre. With further characterization of EEG changes in the preictal state, future AEEG recording may be coupled with a seizure anticipation device, providing a time window within which therapeutic intervention may prevent a seizure.

 

Electromyography (EMG)

Electromyography, in which the electric activity produced by muscles is studied:  This methods help to diagnosis of disease which affect the lower motor neuron, neuromuscular junction, or skeletal muscle fibers.  Iormal muscle at rest no electric activity is detected, but during voluntary contraction the action potentials of motor units appear. In the presence of disease of the motor unit, electric activity of various types may appear in the resting muscle and the action potentials of motor units may have abnormal forms and patterns of activity. Types of abnormal muscle fibers response: «positive waves», «myotonic discharge», «bizarre repetitive potential», «fibrillation», «fasciculation», «repetitive discharge», «muscle cramp».

 

 

Ultrasonic doplerography – finds out the absence or presence of stenosis and occlusions of magistral arteries of head and neck.

 

 

RADIOLOGICAL EXAMINATION OF THE BRAIN AND SPINAL CORD

 

Roentgenography of the spinal column (spondilography)

Plain roentgenograms should always be obtained first, for they can provide diagnostic information quickly and economically. Descriptions of some of the spinal disorders that may be identified by means of a plain roentgenogram follow. Diffuse widening of the spinal canal, scoliosis, kyphosis, multiple vertebral anomalies, spondilolysis, spondilolistesis, osteoporosis, ostheochondrosis, and traumatic lesion of the spinal column.

 

Roentgenography of the scull (RG – cranio graphy)

To find out the signs of the increased intracranial pressure (separation of the cranial sutures in children, the bones of the calvarium may be thinned, demineralization of the posterior clinoid processes and the dorsum of the sella turcica), destruction of the born. Meningiomas often are associated with hyperostosis of bone. Acoustic neuroma often causes erosion of the internal auditory canal. Pituitary tumors produce characteristic enlargement of the sella when they attain sufficient size. Erosion of the clinoid processes and dorsum of the sella may be apparent, and at times the tumor may erode through the floor of the sella into the sphenoid sinus. Occasionally an intracellar aneurysm will produce a similar appearance.

      The usual set of skull films comprises a series made AP, PA (in several degrees of sagittal flexion of the neck), lateral (each side in turn close to the plate), as well as one of the basilar projections in which the ray is directed so that it superimposes the complex basilar structures upon the less complex calvarial cap. The lateral view of the skull shows the two halves of the coronal suture superimposed. The two parts of the lambdoidal suture are seen. Sutures usually remain visible throughout life, distinguishable from fracture lines by their serpiginous character and white margins, while a fracture will be more linear, not at all marginated, and usually more radiolucent. Study the normal skull films on the next slayds.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Normal pituitary fossa:

The white line forming the floor and the dorsum sellae.                   Pituitary tumour causing enlargement of the pituitary fossa with a                      

                                                                                                                      sloping floor. The floor appears as a double line on the lateral view

                                                                                                                      (arrows).

      Traumatic brain injuries include concussion, contusion, skull fracture, and hemorrhage, which may be epidural, subdural, subarachnoid, or intraparenchymal. Epidural hematoma results from rupture of a meningeal artery and follows a hyperacute course, whereas subdural hematoma results from rupture of bridging veins and follows an acute or a chronic course, depending on the severity of the injury. Trauma of the spinal cord produces a variety of neurologic deficits not only from direct neurologic trauma, but also from direct and de­layed damage to the vasculature, with resultant paraplegia or quadriplegia, depending on the level of injury.

PA projection with fractures both linear and depressed. A plate of bone seen in tangent (between the arrows) is slightly depressed. This is not a simple linear fracture but a comminuted one, therefore. Note fillings in the teeth. Identify: odontoid seen through the nose, frontal sinuses, petrous tips with internal auditory canals seen through orbits.

 

 

Pneumocephalography

To enable to visualization of the various portion of the ventricular and subarachnoid system.  The patient seated straddling the chair, lumbar puncture is performed. Then the doctor brings in 20 – 35 sm³ of air in the subarachnoid system. This method is used for diagnostic tumors and inflammatory diseases.

 

Cerebral angiography

It is the method of roentgenologic visualization of the vascular system of the brain during the injection of radiopaque material into the arterial blood stream. A complete angiogram includes the arterial, capillary, and venous phases and is obtained by making rapid, successive roentgenography exposure after injection of the contrast medium. The arterial phase outlines the characteristics of the surface of the brain, whereas the venous phase demonstrates the deep cerebral structures. Secular’s aneurysms, arteriovenous malformations, tumors of blood vessels, and occlusive vascular disease lend themselves well to angiographic demonstration.

 

Computerized transaxial tomography (CT-scan)

It’s a recently developed radiographic method, detects the X-ray density of many cranial and

intracra nial structures and permits their visualization. Its scan the heard in a series of horizontal slices.

n      The newer imaging modalities have had a greater impact on the diagnosis of diseases of the skull, spine and central nervous system than on any other body system. Computed tomography (CT) and magnetic resonance imaging (MRI) have become the standard investigations for most disorders of the brain. Plain films are still the initial investigation for disorders of the bones of the skull – particularly fractures, but otherwise have limited uses. Radionuclide imaging has been almost entirely replaced by CT and MRI. Arteriography is now limited to demonstrating arterial stenoses, aneurysms and some arteriovenous malformations.

 

 

 

 

 

 

Large midline tumour meningioma (arrow) beneath the frontal lobes

 

 

Glioma, CT scan, post i.v. contrast

 

 

 

 

 

 

 

 

 

 

 

 

Metastasis

 

 

Magnetic resonance imaging (MRI) is a noninvasive medical test that helps physicians diagnose and treat medical conditions.

MRI uses a powerful magnetic field, radio frequency pulses and a computer to produce detailed pictures of organs, soft tissues, bone and virtually all other internal body structures. The images can then be examined on a computer monitor, transmitted electronically, printed or copied to a CD. MRI does not use ionizing radiation (x-rays).

Detailed MR images allow physicians to evaluate various parts of the body and determine the presence of certain diseases.

Currently, MRI is the most sensitive imaging test of the head (particularly in the brain) in routine clinical practice.

MR imaging of the head is performed for a number of abrupt onset or long-standing symptoms. It can help diagnose conditions such as:

·         brain tumors

·         stroke

·         infections

·         developmental anomalies

·         hydrocephalus — dilatation of fluid spaces within the brain (ventricles)

·         causes of epilepsy (seizure)

·         hemorrhage in selected trauma patients

·         certain chronic conditions, such as multiple sclerosis

·         disorders of the eye and inner ear

·         disorders of pituitary gland

·         vascular problems, such as an aneurysm (a bubble-like expansion of the vessel), arterial occlusion (blockage) or venous thrombosis (a blood clot within a vein)

Physicians also use the MR examination to detect brain abnormalities in patients with dementia, a disorder that can cause confusion or memory loss.

Contraindications for MRI

Relative contraindications for MRI include the following:

• Metallic implants

• Claustrophobia

• Pacemakers

• MR-incompatible prosthetic heart valves

• Contrast allergy

Patients with metallic implants may have a variety of potential complications, such as heating and pacemaker malfunction and its consequences. For patients with a metallic implant, checking with the manufacturer regarding its MR compatibility is advisable if such information is not available elsewhere.

Claustrophobic patients may be unable to complete the sequence of MRI. In selected patients, mild sedation or imaging in an open MR system may be attempted. However, most open MR scanners provide lesser-quality images.

Rarely, patients may be allergic to the contrast agent (eg, gadolinium) used in MRI.

In the presence of any of these contraindications, a regular radiograph may be indicated.

Diffusion-Weighted Imaging

Diffusion-weighted imaging (DWI) is sensitive to the microscopic random motion of the water molecule protons, a value known as the apparent diffusion coefficient (ADC), which is measured and captured by this type of imaging. The water molecules move in the direction of the magnetic field gradient; they accumulate a phase shift in their transverse magnetization relative to that of a stationary one, and this phase shift is directly related to the signal attenuation of the image. (See the image below.)

The diffusion-weighted MRI reveals a region of hypointensity in the distribution of the right middle cerebral artery. Flanking the anterior and posterior regions of this abnormality are regions of hyperintensities, which represent regions of new infarct. The contiguity of these regions suggests that they are extensions of the old infarct.

Numerous studies have shown that ADCs in ischemic areas are lower by 50% or more compared with those of normal brain areas, and they appear as bright areas (ie, hyperintensities) on DWI (see the image below). Studies have demonstrated that changes in the ADC occur as early as 10 minutes following the onset of ischemia.

Magnetic resonance imaging in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: Apparent diffusion coefficient (ADC) map obtained from the same patient at the same time.

Cytotoxic edema appears following sodium/potassium pump failure, which results from energy metabolism failure due to ischemic insult; this occurs within minutes of the onset of ischemia and produces an increase in brain-tissue water of up to 3-5%. Reduction in intracellular and extracellular water molecule movement is the presumed explanation for the drop in ADC values.

The diffusion of water molecules is guarded by biologic barriers in the brain tissue (eg, cell membranes and cellular organelles). The behavior of water molecules is not symmetrical and may show uneven distribution of the ADC when measured in one direction; this uneven distribution may give a false impression of a lesion. ADC values are measured in several directions (3, 6, or more), and ADC maps are created to produce a direction-insensitive measurement of the diffusion. When the ADC is measured in 6 or more directions, the diffusion motion of all the water molecules (ie, ADC tensor matrix) can be calculated to create what is called full-diffusion tensor mapping, which can also be used to visualize white-matter tracts.

Reduction in the ADC also occurs in other conditions, such as global ischemia, hypoglycemia, and status epilepticus; it should always be evaluated in relation to the clinical condition of the patient.

Human studies have demonstrated that damage in the areas showing decreased ADC levels is very rarely reversible (in contrast to that in animal models), although a few studies have indicated that intra-arterial thrombolysis may occasionally result in the disappearance of the diffusion defect.

The technique most commonly used to acquire DWI is an ultrafast one, echo-planar imaging (EPI); this technique decreases scanning time significantly and eliminates movement artifacts.

The acute drop in ADC is gradually normalized to baseline at 5-10 days after ischemia (pseudonormalization); it even exceeds normal levels as time passes, helping in some cases to differentiate acute, subacute, and chronic lesions.

DWI is very sensitive and relatively specific in detecting acute ischemic stroke. DWI findings have shown high levels of diagnostic accuracy; however, studies have demonstrated that small brainstem lacunar infarctions may escape detection. Normal DWI in patients with strokelike symptoms should trigger further investigation for a nonischemic cause of the symptoms.

DWI has been shown to reveal diffusion abnormalities in almost 50% of patients with clinically defined transient ischemic attacks (TIAs); it tends to be of higher yield at increasing time intervals from the onset of stroke symptoms.

Perfusion-Weighted Imaging

With perfusion-weighted imaging (PWI), information about the perfusion status of the brain is available. The most commonly used technique is bolus-contrast tracking (other techniques include blood oxygen level and arterial spin tagging). The imaging is based on the monitoring of a nondiffusible contrast material (gadolinium) passing through brain tissue.

The signal intensity declines as contrast material passes through the infarcted area and returns to normal as it exits this area. A curve is derived from this tracing data (ie, signal washout curve), which represents and estimates the cerebral blood volume (CBV).

An arterial input function can be derived by measuring an artery in lower brain slices or by measuring gadolinium concentration that is proportional to the changes in T2 when gadolinium is used at low doses (< 3 mg/kg). Based on this arterial input function, quantitative maps of cerebral blood flow (CBF), CBV, mean transit time (MTT), time to peak (TTP), and various other hemodynamic parameters can be obtained. Considerable debate surrounds the choice of which PWI parameter should be used. Most centers in the United States use time domain parameters, such as MTT or TTP.

The use of DWI and PWI together has been shown to be superior to the use of conventional MRI in early phases and up to 48 hours after the onset of stroke. Using a combination of DWI and PWI is very important, because together they provide information about the location and extent of infarction within minutes of onset; when performed in series, they can provide information about the pattern of evolution of the ischemic lesion. This information may be of great importance in choosing the appropriate treatment modality and in predicting the outcome and prognosis.^[1]

The lesion usually enlarges on serial DWI over a period of several days. It has been suggested that this enlargement can be halted if reperfusion (ie, resolution of original PWI lesion) occurs early enough. Lesions that are not large on initial PWI do not show this enlargement.

The diffusion-perfusion mismatch, ie, the difference in size between lesions captured by DWI and PWI, usually represents the ischemic penumbra (see the image below), which is the region of incomplete ischemia that lies next to the core of the infarction.^[2] The ischemic penumbra is regarded as an area that is viable but under ischemic threat; it can be saved if appropriate intervention is promptly instituted. The viability of this region could extend up to 48 hours after the onset of stroke.

Magnetic resonance imaging in acute stroke. Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean transfer time (MTT) map of the same patient.

Determining the volume of the ischemic penumbra may be very useful in identifying patients who would benefit from thrombolytic therapy and perhaps even conventional treatments, such as carotid endarterectomy or blood pressure elevation. It could also aid in evaluating the risk-to-benefit ratio of using such treatments in stroke patients.

Drawbacks to diffusion-perfusion mismatch are mainly methodologic and include the following:

• Lack of anatomic match between diffusion- and perfusion-weighted abnormality

• Variable sensitivity of perfusion-weighted image based on T_max delay

• Visual versus quantitative estimation of mismatch

One limitation of these techniques is in the detection of acute intracerebral hemorrhages; early studies demonstrated that susceptibility imaging could be sensitive in the detection of acute intracerebral hemorrhage. Gradient-recalled echo (GRE) imaging sequences demonstrated the most favorable sensitivity in detecting susceptibility dephasing associated with chronic intracerebral hemorrhages.

DWI and PWI together represent the most exciting areas in MRI for their potential ability to detect early changes (ie, within minutes of the stroke). They are currently used in the evaluation of thrombolytic and neuroprotective therapy in acute stroke clinical trials.

Brain tumor on MRI appear either hypo- (darker than brain tissue) or isointense (same intensity as brain tissue) on T1-weighted scans, or hyperintense (brighter than brain tissue) on T2-weighted MRI, although the appearance is variable.

• Contrast agent uptake, sometimes in characteristic patterns, can be demonstrated on either CT or MRI-scans in most malignant primary and metastatic brain tumors.

• Perifocal edema, or pressure-areas, or where the brain tissue has been compressed by an invasive process also appears hyperintense on T2-weighted MRI, they might indicate the presence a diffuse neoplasm (unclear outline)

 

Brain metastasis in the right cerebral hemisphere from lung cancer shown on T1-weighted magnetic resonance imaging with intravenous contrast

Brain tumor

Widespread use of MRI (magnetic resonance imaging) has revolutionized the ability to diagnose multiple sclerosis. Disease-related changes in the brain or spinal cord are detected by MRI in more than 90% of people suspected of having MS.

Multiple sclerosis

 

Multiple sclerosis

Multiple sclerosis, spinal form

Coronal fluid-attenuated inversion recovery (FLAIR) MRI in a patient with multiple sclerosis demonstrates periventricular high–signal intensity lesions, which exhibit a typical distribution for multiple sclerosis. FLAIR MRI is a highly sensitive sequence for lesion detection, particularly supratentorially.

Axial T2-weighted MRI in a patient with multiple sclerosis demonstrates numerous white matter plaques in a callosal and pericallosal white matter distribution.

 

Students’ Practical Study Program

Step I. Aim: To study the electrophysiological and the roentgenologic methods of examination of neurological patients. Students must get acquainted with apparatus in the department of functional diagnostic.

Step II. Aim: To estimate the parameters of the electrophysiological and the roentgenologic methods of examination of neurological patients. Students must know the normal parameters of the electrophysiological and the roentgenologic methods.

 

 

Step III. Aim: To make topical and clinical diagnosis. For this aim it’s necessary to use algorithm of differential diagnosis, which is in methodological indication for students.